INTRODUCTION

The main cause of peptic ulcers, chronic gastritis and gastric neoplasms is Helicobacter pylori (H. pylori) infection. The International Agency for Research on Cancer[1,2] first classified this bacterium as a group I carcinogen. Several putative virulence-associated factors contribute to its pathogenesis[3]. Virulence markers of H. pylori are intermittently associated with diseases. To effectively treat H. pylori associated diseases, the need to eradicate H. pylori in infected individuals remains the best option. This infection is difficult to eradicate and therefore it is necessary to administer a proton-pump inhibitor (PPI)[4] and group several antibiotics together. H. pylori is sensitive to several antibiotics, i.e., clarithromycin, amoxicillin, metronidazole and tetracycline[5], however, alone these antibiotics cannot eradicate the microorganism[6]. The widespread treatment of amoxicillin, clarithromycin and omeprazole at present, is hardly effective due to increasing resistance to antibiotics. The efficacy of a particular therapy may vary due to patient compromise, age, local antibiotic guidelines, food and hygiene[7].

CRANBERRY

Vaccinium macrocarpon, also known as cranberry is a natural fruit. Studies have shown drinking cranberry juice can in part attenuate H. pylori infection. Cranberries are indigenous to North America and have been widely developed commercially in states, i.e., Wisconsin, Massachusetts, and New Jersey. Cranberry juice is successful in inhibiting or treating urinary tract infections (UTIs) due to its capability to avoid adhesion to the lining of the UT. This bacteriostatic characteristic is attributable to proanthocyanidins[8]. Cranberries, a resource of vitamin C may also provide a bacteriostatic effect.

A previous study demonstrated that an integral part of elevated molecular weight of cranberry juice can prevent H. pylori adhesion in vitro to the human gastric mucosa[9,10] and act on specific adhesions. Other adhesions such as BabA, may also be affected[11].

Animal model studies have demonstrated the importance of BabA in associated H. pylori diseases, influencing the severity of the disease[12]. A recent study illustrated that when cranberry juice was fed to mice infected with H. pylori, 80% were cured 24 h following treatment, with an eradication rate of 20%, 4 wk post-treatment[13]. However, the actual process by which cranberry juice affects the colonization of H. pylori and its suppression deserves further exploration.

Several mechanisms have been postulated as causing the inhibitory action of cranberries against H. pylori; among them are adhesion, biofilm formation blocking[14], anti-oxidative and anti-carcinogen activity[15], proliferation suppression[16,17] due to high concentrations of proanthocyanidins[17], urease inhibition[18], inhibition of the H. pylori adhesion to human gastric mucus[19] and even a cytotoxic effect against the germ[20].

Significant positive results in treating H. pylori infections with cranberry juice have been shown in human in vivo studies. Almost a decade ago, cranberries were tested in combination with traditional anti-H. pylori antibiotics such as metronidazole and clarithromycin[21,22] and proved effective in improving eradication rates and suppressing infections in endemic populations. Nevertheless, very few studies have evaluated the possible beneficial effect of cranberries in healing H. pylori infection.

Zhang et al[23]’s 90 d trial of cranberry juice compared to placebo in 189 patients, exhibited an increase in eradication rates of H. pylori. Shmuely et al[24] suggested, following a double-blind randomized clinical study of several hundreds of subjects, that the inclusion of cranberry juice into a standard therapy protocol of amoxicillin, clarithromycin and omeprazole, may improve eradication rates of H. pylori in females. A recent in vivo study[17] showed that the consumption of cranberry juice may assist in managing colonization among asymptomatic children. Further in vivo studies are needed to advance our knowledge of these mechanisms.

GARLIC

The action of oxidation of fresh Allium sativum L. (garlic) has been established. It is mainly due to unpredictable and irritating organosulphur compounds. Fresh garlic kept for a protracted period (until 20 mo) yields an odorless aged garlic extract comprised of unchanging water soluble organosulphur compounds that deter oxidative damage by scavenging free radicals. Garlic, comparable to allium vegetables, includes a wide range of thiosulphinates, i.e., allicin believed to be accountable for antibacterial activity[25]. It has been shown that the discriminate elimination of thiosulphinates or the avoidance of their creation by obstructing alliinase, destroys the garlic’s antibacterial activity[25].

Several studies have revealed that extracts from raw garlic[26] or garlic powder tablets[27] maintains in vitro activity against H. pylori, i.e., steam-distilled garlic oil.

In Cañizares et al[28]’s study of allium sativum extracts; the authors used purple garlic of the “Las Pedroñeras” variety. By using the solvents ethanol and acetone in a stirred tank, it was shown that garlic extracts inhibit H. pylori comparable to commercial materials. The extracted material can be directly applied thus, necessitating an extraction procedure which is simple and economical.

Allicin, associated with Allium sativum is believed accountable for garlic’s bacteriostatic properties. The existence or lack of allicin is critical in inhibiting in-vitro growth of H. pylori[27].

Several studies have proven a diminished gastric cancer risk with a rise in the intake of allium vegetables[29], perhaps producing a positive influence on H. pylori. You et al[30] in a randomized trial of 3365 subjects randomly selected from villages in the Shandong Province of China, a district with high gastric cancer death rates and an occurrence of approximately 67% in individuals infected with H. pylori, tested the outcomes of short-term (once) H. pylori treatment and continuous vitamin or garlic supplements (long-term) in the incidence of progressive precancerous gastric lesions. Individuals aged 35-64 years were randomly assigned to three interventions or placebos: Amoxicillin and omeprazole for 14 d (H. pylori treatment); vitamin C, vitamin E, and selenium for 7.3 years (vitamin supplement); and aged garlic extract and steam-distilled garlic oil for 7.3 years (garlic supplement)[30]. The patients endured an esophagogastroduodenoscopy and biopsy. The frequency of the appearance of precancerous gastric lesions was established by a histopathologic examination of seven biopsy sites[30]. Treatment for H. pylori did not diminish the occurrence of dysplasia or gastric cancer. However, a smaller number of patients receiving treatment for H. pylori rather than a placebo developed gastric cancer. There were no significant favorable disparities when garlic or vitamin supplements were consumed.

In a recent study[31], permanent residents of West China underwent a ¹⁴C-urea breath test (¹⁴C-UBT) used to diagnose H. pylori infection. Of the 8365 participants, 53.1% were diagnosed with H. pylori infection. Those who ate raw garlic had a statistically significant lower level of H. pylori infection than those who did not eat the raw garlic. In this region, raw garlic seemed to reduce the infection.

Salih et al[32] reported that in a Turkish population, consumption of garlic for long periods of time did not affect the occurrence of H. pylori infection. Those ingesting garlic demonstrated a significantly lower antibody titer than the non-garlic groups, suggesting an unintended inhibitory effect on the generation of H. pylori and a possible advancement to more acute diseases. McNulty et al[33]’s in vivo pilot study, failed to show that steam distilled garlic oil, inhibits H. pylori based on in vitro activity. In this study, 20 dyspeptic patients aged 18-75 years, exhibiting H. pylori positive serology, verified by a ¹³C urea breath test, were treated with a 4 mg garlic oil capsule taken with meals, 4 times a day for two weeks.

Negative UBT indicated H. pylori eradication. A 50% fall in ¹³C excess between baseline and follow-up was defined as suppression. There was no verification that by ingesting garlic oil, H. pylori was either eradicated, suppressed or improvement of symptoms.

Aydin et al[34] also reported negative results in a trial using “Ortis” brand “garlic oil” produced by mixing ground garlic cloves with vegetable oil. These negative in vivo results show that garlic oil at these doses does not inhibit H. pylori. Further exploration of the possible beneficial outcomes of garlic oil against H. pylori, is necessary.

CURCUMIN

Curcumin (diferuloylmethane) was ﬁrst chemically classified in 1910 and is generally considered the most active component of the Curcuma longa herb (turmeric). Due to its distinguishing ﬂavor and yellow color similar to curry, it is used as a spice[35]. Its anti-inﬂammatory, antimutagen, antioxidant, and anti- infectious properties have been previously studied[36-41]. The significance of curcumin has been established in in vitro and in vivo studies. Curcumin has been used in healing peptic ulcers as well as preventing H. pylori growth[42-44].

Kundu et al[45] demonstrated that curcumin is capable of eradicating H. pylori in mice. In H. pylori infected human gastric epithelial cells, a dose of curcumin suppressed MMP-3 and -9 expression. Eliminating H. pylori using curcumin, entails significant down regulation of MMP-3 and -9 activities in addition to expression in the cytotoxic associated gene (cag) positive and cag-negative H. pylori-infected gastric tissues. These data indicate that curcumin healing of H. pylori infection includes regulating MMP-3 and -9 activities.

Han et al[46] confirmed that the growth inhibitory activity of curcumin via H. pylori infection is a result of inhibition of the shikimate pathway essential for the production of aromatic amino acids in bacteria, but not in humans. The shikimate pathway is vital for the production of metabolites in bacteria, i.e., aromatic amino acids, folic acid and ubiquinone[47]. The enzymes affected include shikimate dehydrogenase which are innovative drug targets in the development of nontoxic antimicrobial agents[48].

Recently, the effect of curcumin on the formulation of interleukin (IL)-8, IL-1β, tumor necrosis factor (TNF)-α and cyclooxygenase (COX)-2 in gastric mucosa taken from H. pylori-infected gastritis subjects, was investigated by Koosirirat et al[49]. Patients were assigned at random to either a treatment course of Omeprazole, Amoxicillin and Metronidazole (OAM) or curcumin. Gastric biopsies were collected pre and post-treatment. In addition, the level of inflammatory cytokines mRNA were measured using semi-quantitative reverse transcription polymerase chain reaction.

Patients who received OAM treatment found that the eradication rate was significantly higher in these patients than those who ingested curcumin (78.9% vs 5.9%). In the OAM group, the levels of IL-8 mRNA expression significantly worsened after treatment, however, no alterations of other cytokines were found. Thus, only curcumin may have a reduced in-vivo anti-bactericidal effect on H. pylori and on the generation of inflammatory cytokines.

Prucksunand et al[50]’s phase II clinical trial reporting on the results of healing peptic ulcers with long turmeric (Curcuma longa Linn), examined patients with peptic ulcer symptoms. While performing an endoscopy, ulcers measuring 0.5 to 1.5 cm in diameter were found in the duodenal bulb and stomach. An oral dose of 300 mg, 5 times daily of capsule-filled turmeric was given. Treatment after 4 wk, revealed no ulcers in 48% and after another 12 wk of treatment, 76% had no ulcers. Abdominal pain and discomfort sufficiently lessened during the first and second week. The subjects were able to ingest normal foods instead of soft meals. New insights as to the therapeutic effect of curcumin in the treatment of peptic ulcers, encourages the use of curcumin as an alternative therapy. Yet in-vivo evidence that curcumin is active against H. pylori infection is still lacking.

GINGER

Ginger root (Zingiber officinale) is traditionally designed for treating gastrointestinal ailments, i.e., hyperemesis gravidarum, dyspepsia, peptic ulcer, motion sickness and inflammatory disorders[51]. The proximate chemical composition of ginger contains volatile oils (1%-4%), medically active elements of ginger.

Ginger employs anti-oxidant and anti-ulcer[52], anti-inﬂammatory, anti-tumor[53], carminative, diaphonic and digestive, expectorant actions[54]. The phenols found in solvent extracts of ginger are mainly gingerol and zingerone.

Siddaraju et al[55] found that an aqueous extract of ginger can protect the gastric mucosa from stress-induced mucosal lesions and inhibit gastric acid secretion, which can be done by blocking H⁺, K⁺-ATPase action, thus restricting H. pylori growth. Ginger produces anti-oxidant protection against oxidative stress-induced gastric damage, thus, exhibiting anti-oxidative properties in vitro.

Li et al[56] validated and strengthened the association between hyperemesis gravidarum (HG) and H. pylori infection in normal pregnant control subjects and pregnant women with HG. They found positive H. pylori in 1289 (69.6%) HG cases and 1045 (46.2%) H. pylori-positive in the control group. The infection rate of H. pylori was considerably higher in pregnant women with HG compared to the non-HG normal pregnant controls. Analysis of a subgroup revealed that H. pylori infection was a risk factor of HG in other countries, i.e., Oceania, Asia and especially Africa. Karaca et al[57] stated that lower socio-economic status was an important risk factor for H. pylori infected pregnant women with an HG factor.

Other studies have found that certain agents active against H. pylori are very effective in the treatment of hyperemesis[58,59]. The human Chorionic Gonadotropin (hCG) when elevated in pregnancy, concurrently alters the pH in pregnancy. hCG was found to induce gastrointestinal dysmotility, altered humoral as well as cell mediated immunity in pregnancy believed to be the basis for infection.

Several preclinical studies suggest that ginger, an agent linked to gastric and colon carcinogenesis, generates a protective effect against H. pylori[57,58]. Ginger phenolic fractions provide inhibitory effects on the growth of H. pylori, scavenge free radicals, reduce power abilities, protect DNA and inhibit lipid peroxidation[59,60].

Mahady et al[58] reported on the chemo-preventative effects of ginger which directly impede H. pylori growth, particularly CagA+ strains. The authors showed that gingerols and ginger extracts inhibit the development of H. pylori in vitro of 19 clinical strains. In addition, the fraction comprising the gingerols and 6-shogoal was very successful in inhibiting the growth of H. pylori CagA+ strains. This documentation suggests that specific ginger extracts containing gingerols may assist in treating or preventing H. pylori CagA and strains in vivo.

Researchers studying Mongolian gerbils noted that ginger extract prevented and treated H. pylori-induced infection and inflammation[61]. Moreover, additional research was implemented to clarify the in vitro mechanism of the ginger extract. These results confirm the medicinal properties of ginger in Ayurveda and folklore medicines and further advocate that ginger be considered a new therapeutic approach in the treatment of gastric disorders.

PISTACIA GUM

A resin called Chios mastic gum (CMG), produced by the Pistacia lentiscus var. chia. plant, is nurtured predominantly in the southern part of the Greek island of Chios and other Mediterranean countries. However, this plant can be planted or re-planted in other locations around the world, including the northern part of Chios, however, it will not produce resin.

The first mention of mastic was noted by Herodotus in the 5^th century BC. Since 3000 BC, CMG has been used by the Greeks in cooking, cosmetics, and treating gastric illnesses.

In the 1980s, CMG was found to be a potential agent in treating duodenal ulcers in humans[62]. The antibacterial action of CMG was assessed and compared to clinical isolates of H. pylori[63]. Transmission electron microscopy determined CMG’s influence on H. pylori morphology. CMG presents with anti-H. pylori activity due its inducement of protrusions, morphological abnormalities and cellular fragmentation in H. pylori cells[64].

A 2011 study presented proof that CMG prevents H. pylori inflammation by inhibiting neutrophil activation in vitro[65]. Dabos et al[66] confirmed these observations by examining the influence of CMG on H. pylori eradication in H. pylori patients. Mastic gum was well tolerated and the mild side effects were reversible.

It was determined that CMG has bactericidal action against H. pylori in vivo[66]. Paraschos et al[67] found that extracts and elements of CMG were active against H. pylori. After the insoluble polymer was removed, a total mastic extract without polymer was prepared, thus improving solubility and enhancing in vivo activity. The acid fraction generated major triterpenic acids after chromatographic separation, while the neutral fraction generated several triterpenic alcohols and aldehydes.

Employing a panel of 11 H. pylori clinical strains, CMG extracts and isolated pure triterpenic acids were tested for in vitro action. The authors demonstrated that administration of CMG may reduce H. pylori settlement. In addition, the major triterpenic acids found in the acid extract may be responsible for this activity[68].

Other animal studies reported that CMG has no effect on H. pylori[68,69]. Monotherapy of CMG was administered to prove its ability to eliminate H. pylori infection in mice. The results showed that CMG was unable to eradicate H. pylori infection in mice. Also, Loughlin et al[69] reported that CMG failed to suppress or destroy H. pylori infection in humans. Patients with H. pylori infection were treated with 1g of CMG, 4 times daily for 14 d. CMG was found to have no effect on H. pylori status; they all remained H. pylori-positive. It was resolved that despite the anti-H. pylori action in vitro, there seems to be no effect on H. pylori in humans due to CMG[69].

All H. pylori-positive patients, treated with mastic capsules for 7 d remained H. pylori positive[70]. Miyamoto et al[70] and Huwez et al[71] observed that no “antibiotic-like” activity should be anticipated from crude mastic.

It has been shown that mastic has definite antibacterial action via H. pylori. This may partially explain the anti-peptic-ulcer mastic’s properties[62,71]. By examining the effect of anti-H. pylori of the various elements of mastic, researchers may in the future, identify the participating ingredient.

Mastic is inexpensive and widely accessible in third world countries, hence, more in-vivo studies should be performed in developing countries.

CONCLUSION

Compared with the use of antibiotic and PPI treatment, a preventive dietary approach can be very inexpensive in areas with poor health care systems. The food reviewed can be effective in preventing and/or reducing H. pylori infection due to their potent anti-inflammatory activity. The rapid uptake by cells (Table 1) provides the suggested anti-H. pylori mechanisms of the foods and plant extracts.

Table 1 Suggested anti-Helicobacter pylori mechanisms of the foods and plant extracts.

Agentadministered	Major mechanisms	Ref.
Cranberry	Bacteriostatic properties of proanthocyanidins	Howell[8], Gotteland et al[17]
Inhibition of adhesion to the human gastric mucosa in vitro	Burger et al[9], Parente et al[10], Burger et al[19]
Inhibition of adhesion and biofilm formation blocking	Shmuely et al[14]
Anti-oxidative and anti-carcinogen activity	Côté et al[15]
Proliferation suppression	Matsushima et al[16], Gotteland et al[17]
Urease inhibition	Lin et al[18]
Cytotoxic effect	Zafra-Stone et al[20]
Garlic	Antibacterial activity by thiosulphinates	Farbman et al[25]
Curcumin	Suppression of Matrix Metalloproteinase-3 and -9 expression in H. pylori infected human gastric epithelial cells	Kundu et al[45]
Inhibition of the shikimate pathway, necessary for synthesis of aromatic amino acids	Han et al[46]
Effect upon the production of IL-8, IL-1β, tumor necrosis factor-α and cyclooxygenase-2 in gastric mucosa	Koosirirat et al[49]
Ginger	Anti-oxidant and anti-ulcer activity	Yoshikawa et al[52]
Anti-inﬂammatory and anti-tumor activity	Kim et al[53]
Blocking H⁺, K⁺-ATPase action, inhibitory effects on the growth of H. pylori, DNA protection and inhibition of lipid peroxidation	Siddaraju et al[55]
6-gingerol enhances the tumor necrosis factor-related apoptosis by inhibiting nuclear factor kappa B	Ishiguro et al[60]
Directly inhibiting the growth of H. pylori, particularly the CagA+ strains	Mahady et al[58]
Pistacia Gum	Induction of protrusions, morphological abnormalities, and cellular fragmentation in H. pylori cells	Marone et al[64]
Inhibition of neutrophil activation	Choli-Papadopoulou et al[65]
Triterpenic acids present in the acid extract	Paraschos et al[67]

6.	Peterson WL, Graham DY, Marshall B, Blaser MJ, Genta RM, Klein PD, Stratton CW, Drnec J, Prokocimer P, Siepman N. Clarithromycin as monotherapy for eradication of Helicobacter pylori: a randomized, double-blind trial. Am J Gastroenterol. 1993;88:1860-1864. [PubMed] [Cited in This Article: ]

12.	Guruge JL, Falk PG, Lorenz RG, Dans M, Wirth HP, Blaser MJ, Berg DE, Gordon JI. Epithelial attachment alters the outcome of Helicobacter pylori infection. Proc Natl Acad Sci USA. 1998;95:3925-3930. [PubMed] [Cited in This Article: ]

31.	Tang HR, Fan YJ, Liu S. Helicobacter pylori infection and associated risk factors in Chengdu. Sichuan Daxue Xuebao Yixueban. 2014;45:823-826. [PubMed] [Cited in This Article: ]

32.	Salih BA, Abasiyanik FM. Does regular garlic intake affect the prevalence of Helicobacter pylori in asymptomatic subjects? Saudi Med J. 2003;24:842-845. [PubMed] [Cited in This Article: ]

34.	Aydin A, Ersöz G, Tekesin O, Akçiçek E, Tuncyurek M, Batur Y. Does garlic oil have a role in the treatment of Helicobacter pylori infection? Turk Gastroenteroloji Dergisi. 1997;8:181-184. [Cited in This Article: ]

36.

Egan ME, Pearson M, Weiner SA, Rajendran V, Rubin D, Glöckner-Pagel J, Canny S, Du K, Lukacs GL, Caplan MJ. Curcumin, a major constituent of turmeric, corrects cystic fibrosis defects. Science. 2004;304:600-602. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 414] [Cited by in F6Publishing: 439] [Article Influence: 21.8] [Reference Citation Analysis (0)]

43.	Foryst-Ludwig A, Neumann M, Schneider-Brachert W, Naumann M. Curcumin blocks NF-kappaB and the motogenic response in Helicobacter pylori-infected epithelial cells. Biochem Biophys Res Commun. 2004;316:1065-1072. [PubMed] [Cited in This Article: ]

46.	Han C, Wang L, Yu K, Chen L, Hu L, Chen K, Jiang H, Shen X. Biochemical characterization and inhibitor discovery of shikimate dehydrogenase from Helicobacter pylori. FEBS J. 2006;273:4682-4692. [PubMed] [Cited in This Article: ]

48.	Coggins JR, Abell C, Evans LB, Frederickson M, Robinson DA, Roszak AW, Lapthorn AP. Experiences with the shikimate-pathway enzymes as targets for rational drug design. Biochem Soc Trans. 2003;31:548-552. [PubMed] [Cited in This Article: ]

50.	Prucksunand C, Indrasukhsri B, Leethochawalit M, Hungspreugs K. Phase II clinical trial on effect of the long turmeric (Curcuma longa Linn) on healing of peptic ulcer. Southeast Asian J Trop Med Public Health. 2001;32:208-215. [PubMed] [Cited in This Article: ]

52.

Yoshikawa M, Yamaguchi S, Kunimi K, Matsuda H, Okuno Y, Yamahara J, Murakami N. Stomachic principles in ginger. III. An anti-ulcer principle, 6-gingesulfonic acid, and three monoacyldigalactosylglycerols, gingerglycolipids A, B, and C, from Zingiberis Rhizoma originating in Taiwan. Chem Pharm Bull (Tokyo). 1994;42:1226-1230. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 90] [Cited by in F6Publishing: 93] [Article Influence: 3.1] [Reference Citation Analysis (0)]

57.	Karaca C, Güler N, Yazar A, Camlica H, Demir K, Yildirim G. Is lower socio-economic status a risk factor for Helicobacter pylori infection in pregnant women with hyperemesis gravidarum? Turk J Gastroenterol. 2004;15:86-89. [PubMed] [Cited in This Article: ]

58.	Mahady GB, Pendland SL, Yun GS, Lu ZZ, Stoia A. Ginger (Zingiber officinale Roscoe) and the gingerols inhibit the growth of Cag A+ strains of Helicobacter pylori. Anticancer Res. 2003;23:3699-3702. [PubMed] [Cited in This Article: ]

60.	Ishiguro K, Ando T, Maeda O, Ohmiya N, Niwa Y, Kadomatsu K, Goto H. Ginger ingredients reduce viability of gastric cancer cells via distinct mechanisms. Biochem Biophys Res Commun. 2007;362:218-223. [PubMed] [Cited in This Article: ]

62.	Al-Habbal MJ, Al-Habbal Z, Huwez FU. A double-blind controlled clinical trial of mastic and placebo in the treatment of duodenal ulcer. Clin Exp Pharmacol Physiol. 1984;11:541-544. [PubMed] [Cited in This Article: ]

64.	Marone P, Bono L, Leone E, Bona S, Carretto E, Perversi L. Bactericidal activity of Pistacia lentiscus mastic gum against Helicobacter pylori. J Chemother. 2001;13:611-614. [PubMed] [Cited in This Article: ]

67.

Paraschos S, Magiatis P, Mitakou S, Petraki K, Kalliaropoulos A, Maragkoudakis P, Mentis A, Sgouras D, Skaltsounis AL. In vitro and in vivo activities of Chios mastic gum extracts and constituents against Helicobacter pylori. Antimicrob Agents Chemother. 2007;51:551-559. [PubMed] [Cited in This Article: ]

68.	Bebb JR, Bailey-Flitter N, Ala’Aldeen D, Atherton JC. Mastic gum has no effect on Helicobacter pylori load in vivo. J Antimicrob Chemother. 2003;52:522-523. [PubMed] [Cited in This Article: ]

69.	Loughlin MF, Ala’Aldeen DA, Jenks PJ. Monotherapy with mastic does not eradicate Helicobacter pylori infection from mice. J Antimicrob Chemother. 2003;51:367-371. [PubMed] [Cited in This Article: ]

71.	Huwez FU, Al-Habbal MJ. Mastic in treatment of benign gastric ulcers. Gastroenterol Jpn. 1986;21:273-274. [PubMed] [Cited in This Article: ]

||||I|||| * Home * English + English 简体中文 * Sign In + BPG Management System + F6Publishing-Submit a Manuscript + F6Publishing-世界华人消化杂志在线投稿 + RCA Management System * Help Desk * Journals Advanced Search BPG is committed to discovery and dissemination of knowledge * About the Journal * Submit a Manuscript * Current Issue * Search All Articles This Article * Abstract * Core Tip * Full Article (PDF) * Full Article (WORD) * Full Article (HTML) * Audio * PubMed Central * PubMed * CrossRef * Google Scholar * Similar Articles (365) * Timeline of Article Publication (1) * Article Quality Tracking (0) * Reference Citation Analysis (2) * * Send to Friends (0) * * * * * Academic Content and Language Evaluation of This Article CrossCheck and Google Search of This Article Academic Rules and Norms of This Article Citation of this article Corresponding Author of This Article Checklist of Responsibilities for the Scientific Editor of This Article Publishing Process of This Article Research Domain of This Article Article-Type of This Article Open-Access Policy of This Article Times Cited Counts in Google of This Article Number of Hits and Downloads for This Article * Total Article Views (12361) All Articles published online Item Count PDF 1449 WORD 361 HTML 7858 Scan QR Codes (HTML) 163 Scan QR Codes (PDF) 90 Tables (1-1) 70 Sum=9991 Publishing Process of This Article Item Count Browse 1025 Download 1598 Sum=2623 May 6, 2016 (publication date) through Feb 7, 2023 Times Cited of This Article * Times Cited (11) Journal Information of This Article Publication Name World Journal of Gastrointestinal Pharmacology and Therapeutics ISSN 2150-5349 Publisher of This Article Baishideng Publishing Group Inc, 7041 Koll Center Parkway, Suite 160, Pleasanton, CA 94566, USA Topic Highlight Open Access Copyright ©The Author(s) 2016. Published by Baishideng Publishing Group Inc. All rights reserved. World J Gastrointest Pharmacol Ther. May 6, 2016; 7(2): 171-178 Published online May 6, 2016. doi: 10.4292/wjgpt.v7.i2.171 Non-pharmacological treatment of Helicobacter pylori Haim Shmuely, Noam Domniz, Jacob Yahav Haim Shmuely, Jacob Yahav, Department Medicine D, Kaplan Medical Center, Rehovot 76100, Israel Noam Domniz, Sheba Medical Center, Tel-Hashomer, Ramat Gan 52506, Israel Author contributions: Shmuely H, Domniz N and Yahav J contributed equally to this work. Conflict-of-interest statement: The authors have no conflicts of interest to report. Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/ Correspondence to: Dr. Haim Shmuely, MD, Head, Department Medicine D, Kaplan Medical Center, Pasternak St., Rehovot 76100, Israel. hshmuely@zahav.net.il Telephone: +972-8-9441996 Fax: +972-8-9441866 Received: April 28, 2015 Peer-review started: May 6, 2015 First decision: September 8, 2015 Revised: January 13, 2016 Accepted: February 14, 2016 Article in press: February 16, 2016 Published online: May 6, 2016 Abstract Many food and plant extracts have shown in vitro anti-Helicobacter pylori (H. pylori) activity, but are less effective in vivo. The anti-H. pylori effects of these extracts are mainly permeabilitization of the membrane, anti-adhesion, inhibition of bacterial enzymes and bacterial grown. We, herein, review treatment effects of cranberry, garlic, curcumin, ginger and pistacia gum against H. pylori in both in vitro, animal studies and in vivo studies. Key Words: Helicobacter pylori , Cranberry , Garlic , Curcumin , Ginger , Pistacia gum Core tip: Helicobacter pylori (H. pylori) infection is difficult to eradicate and therefore, it is necessary to combine several antibiotics as well as administering a proton-pump inhibitor. Many food and plant extracts have demonstrated in vitro antibacterial activity, however, in in vivo, they are less effective. The food reviewed, herein, can be effective in preventing and/or reducing H. pylori infection. A preventive dietary approach can be very inexpensive in areas with poor health care systems. * Citation: Shmuely H, Domniz N, Yahav J. Non-pharmacological treatment of Helicobacter pylori. World J Gastrointest Pharmacol Ther 2016; 7(2): 171-178 * URL: https://www.wjgnet.com/2150-5349/full/v7/i2/171.htm * DOI: https://dx.doi.org/10.4292/wjgpt.v7.i2.171 INTRODUCTION The main cause of peptic ulcers, chronic gastritis and gastric neoplasms is Helicobacter pylori (H. pylori) infection. The International Agency for Research on Cancer[1,2] first classified this bacterium as a group I carcinogen. Several putative virulence-associated factors contribute to its pathogenesis[3]. Virulence markers of H. pylori are intermittently associated with diseases. To effectively treat H. pylori associated diseases, the need to eradicate H. pylori in infected individuals remains the best option. This infection is difficult to eradicate and therefore it is necessary to administer a proton-pump inhibitor (PPI)[4] and group several antibiotics together. H. pylori is sensitive to several antibiotics, i.e., clarithromycin, amoxicillin, metronidazole and tetracycline[5], however, alone these antibiotics cannot eradicate the microorganism[6]. The widespread treatment of amoxicillin, clarithromycin and omeprazole at present, is hardly effective due to increasing resistance to antibiotics. The efficacy of a particular therapy may vary due to patient compromise, age, local antibiotic guidelines, food and hygiene[7]. CRANBERRY Vaccinium macrocarpon, also known as cranberry is a natural fruit. Studies have shown drinking cranberry juice can in part attenuate H. pylori infection. Cranberries are indigenous to North America and have been widely developed commercially in states, i.e., Wisconsin, Massachusetts, and New Jersey. Cranberry juice is successful in inhibiting or treating urinary tract infections (UTIs) due to its capability to avoid adhesion to the lining of the UT. This bacteriostatic characteristic is attributable to proanthocyanidins[8]. Cranberries, a resource of vitamin C may also provide a bacteriostatic effect. A previous study demonstrated that an integral part of elevated molecular weight of cranberry juice can prevent H. pylori adhesion in vitro to the human gastric mucosa[9,10] and act on specific adhesions. Other adhesions such as BabA, may also be affected[11]. Animal model studies have demonstrated the importance of BabA in associated H. pylori diseases, influencing the severity of the disease[12]. A recent study illustrated that when cranberry juice was fed to mice infected with H. pylori, 80% were cured 24 h following treatment, with an eradication rate of 20%, 4 wk post-treatment[13]. However, the actual process by which cranberry juice affects the colonization of H. pylori and its suppression deserves further exploration. Several mechanisms have been postulated as causing the inhibitory action of cranberries against H. pylori; among them are adhesion, biofilm formation blocking[14], anti-oxidative and anti-carcinogen activity[15], proliferation suppression[16,17] due to high concentrations of proanthocyanidins[17], urease inhibition[18], inhibition of the H. pylori adhesion to human gastric mucus[19] and even a cytotoxic effect against the germ[20]. Significant positive results in treating H. pylori infections with cranberry juice have been shown in human in vivo studies. Almost a decade ago, cranberries were tested in combination with traditional anti-H. pylori antibiotics such as metronidazole and clarithromycin[21,22] and proved effective in improving eradication rates and suppressing infections in endemic populations. Nevertheless, very few studies have evaluated the possible beneficial effect of cranberries in healing H. pylori infection. Zhang et al[23]’s 90 d trial of cranberry juice compared to placebo in 189 patients, exhibited an increase in eradication rates of H. pylori. Shmuely et al[24] suggested, following a double-blind randomized clinical study of several hundreds of subjects, that the inclusion of cranberry juice into a standard therapy protocol of amoxicillin, clarithromycin and omeprazole, may improve eradication rates of H. pylori in females. A recent in vivo study[17] showed that the consumption of cranberry juice may assist in managing colonization among asymptomatic children. Further in vivo studies are needed to advance our knowledge of these mechanisms. GARLIC The action of oxidation of fresh Allium sativum L. (garlic) has been established. It is mainly due to unpredictable and irritating organosulphur compounds. Fresh garlic kept for a protracted period (until 20 mo) yields an odorless aged garlic extract comprised of unchanging water soluble organosulphur compounds that deter oxidative damage by scavenging free radicals. Garlic, comparable to allium vegetables, includes a wide range of thiosulphinates, i.e., allicin believed to be accountable for antibacterial activity[25]. It has been shown that the discriminate elimination of thiosulphinates or the avoidance of their creation by obstructing alliinase, destroys the garlic’s antibacterial activity[25]. Several studies have revealed that extracts from raw garlic[26] or garlic powder tablets[27] maintains in vitro activity against H. pylori, i.e., steam-distilled garlic oil. In Cañizares et al[28]’s study of allium sativum extracts; the authors used purple garlic of the “Las Pedroñeras” variety. By using the solvents ethanol and acetone in a stirred tank, it was shown that garlic extracts inhibit H. pylori comparable to commercial materials. The extracted material can be directly applied thus, necessitating an extraction procedure which is simple and economical. Allicin, associated with Allium sativum is believed accountable for garlic’s bacteriostatic properties. The existence or lack of allicin is critical in inhibiting in-vitro growth of H. pylori[27]. Several studies have proven a diminished gastric cancer risk with a rise in the intake of allium vegetables[29], perhaps producing a positive influence on H. pylori. You et al[30] in a randomized trial of 3365 subjects randomly selected from villages in the Shandong Province of China, a district with high gastric cancer death rates and an occurrence of approximately 67% in individuals infected with H. pylori, tested the outcomes of short-term (once) H. pylori treatment and continuous vitamin or garlic supplements (long-term) in the incidence of progressive precancerous gastric lesions. Individuals aged 35-64 years were randomly assigned to three interventions or placebos: Amoxicillin and omeprazole for 14 d (H. pylori treatment); vitamin C, vitamin E, and selenium for 7.3 years (vitamin supplement); and aged garlic extract and steam-distilled garlic oil for 7.3 years (garlic supplement)[30]. The patients endured an esophagogastroduodenoscopy and biopsy. The frequency of the appearance of precancerous gastric lesions was established by a histopathologic examination of seven biopsy sites[30]. Treatment for H. pylori did not diminish the occurrence of dysplasia or gastric cancer. However, a smaller number of patients receiving treatment for H. pylori rather than a placebo developed gastric cancer. There were no significant favorable disparities when garlic or vitamin supplements were consumed. In a recent study[31], permanent residents of West China underwent a 14C-urea breath test (14C-UBT) used to diagnose H. pylori infection. Of the 8365 participants, 53.1% were diagnosed with H. pylori infection. Those who ate raw garlic had a statistically significant lower level of H. pylori infection than those who did not eat the raw garlic. In this region, raw garlic seemed to reduce the infection. Salih et al[32] reported that in a Turkish population, consumption of garlic for long periods of time did not affect the occurrence of H. pylori infection. Those ingesting garlic demonstrated a significantly lower antibody titer than the non-garlic groups, suggesting an unintended inhibitory effect on the generation of H. pylori and a possible advancement to more acute diseases. McNulty et al[33]’s in vivo pilot study, failed to show that steam distilled garlic oil, inhibits H. pylori based on in vitro activity. In this study, 20 dyspeptic patients aged 18-75 years, exhibiting H. pylori positive serology, verified by a 13C urea breath test, were treated with a 4 mg garlic oil capsule taken with meals, 4 times a day for two weeks. Negative UBT indicated H. pylori eradication. A 50% fall in 13C excess between baseline and follow-up was defined as suppression. There was no verification that by ingesting garlic oil, H. pylori was either eradicated, suppressed or improvement of symptoms. Aydin et al[34] also reported negative results in a trial using “Ortis” brand “garlic oil” produced by mixing ground garlic cloves with vegetable oil. These negative in vivo results show that garlic oil at these doses does not inhibit H. pylori. Further exploration of the possible beneficial outcomes of garlic oil against H. pylori, is necessary. CURCUMIN Curcumin (diferuloylmethane) was ﬁrst chemically classified in 1910 and is generally considered the most active component of the Curcuma longa herb (turmeric). Due to its distinguishing ﬂavor and yellow color similar to curry, it is used as a spice[35]. Its anti-inﬂammatory, antimutagen, antioxidant, and anti- infectious properties have been previously studied[36 - 41]. The significance of curcumin has been established in in vitro and in vivo studies. Curcumin has been used in healing peptic ulcers as well as preventing H. pylori growth[42 - 44]. Kundu et al[45] demonstrated that curcumin is capable of eradicating H. pylori in mice. In H. pylori infected human gastric epithelial cells, a dose of curcumin suppressed MMP-3 and -9 expression. Eliminating H. pylori using curcumin, entails significant down regulation of MMP-3 and -9 activities in addition to expression in the cytotoxic associated gene (cag) positive and cag-negative H. pylori-infected gastric tissues. These data indicate that curcumin healing of H. pylori infection includes regulating MMP-3 and -9 activities. Han et al[46] confirmed that the growth inhibitory activity of curcumin via H. pylori infection is a result of inhibition of the shikimate pathway essential for the production of aromatic amino acids in bacteria, but not in humans. The shikimate pathway is vital for the production of metabolites in bacteria, i.e., aromatic amino acids, folic acid and ubiquinone[47]. The enzymes affected include shikimate dehydrogenase which are innovative drug targets in the development of nontoxic antimicrobial agents[48]. Recently, the effect of curcumin on the formulation of interleukin (IL)-8, IL-1β, tumor necrosis factor (TNF)-α and cyclooxygenase (COX)-2 in gastric mucosa taken from H. pylori-infected gastritis subjects, was investigated by Koosirirat et al[49]. Patients were assigned at random to either a treatment course of Omeprazole, Amoxicillin and Metronidazole (OAM) or curcumin. Gastric biopsies were collected pre and post-treatment. In addition, the level of inflammatory cytokines mRNA were measured using semi-quantitative reverse transcription polymerase chain reaction. Patients who received OAM treatment found that the eradication rate was significantly higher in these patients than those who ingested curcumin (78.9% vs 5.9%). In the OAM group, the levels of IL-8 mRNA expression significantly worsened after treatment, however, no alterations of other cytokines were found. Thus, only curcumin may have a reduced in-vivo anti-bactericidal effect on H. pylori and on the generation of inflammatory cytokines. Prucksunand et al[50]’s phase II clinical trial reporting on the results of healing peptic ulcers with long turmeric (Curcuma longa Linn), examined patients with peptic ulcer symptoms. While performing an endoscopy, ulcers measuring 0.5 to 1.5 cm in diameter were found in the duodenal bulb and stomach. An oral dose of 300 mg, 5 times daily of capsule-filled turmeric was given. Treatment after 4 wk, revealed no ulcers in 48% and after another 12 wk of treatment, 76% had no ulcers. Abdominal pain and discomfort sufficiently lessened during the first and second week. The subjects were able to ingest normal foods instead of soft meals. New insights as to the therapeutic effect of curcumin in the treatment of peptic ulcers, encourages the use of curcumin as an alternative therapy. Yet in-vivo evidence that curcumin is active against H. pylori infection is still lacking. GINGER Ginger root (Zingiber officinale) is traditionally designed for treating gastrointestinal ailments, i.e., hyperemesis gravidarum, dyspepsia, peptic ulcer, motion sickness and inflammatory disorders[51]. The proximate chemical composition of ginger contains volatile oils (1%-4%), medically active elements of ginger. Ginger employs anti-oxidant and anti-ulcer[52], anti-inﬂammatory, anti-tumor[53], carminative, diaphonic and digestive, expectorant actions[54]. The phenols found in solvent extracts of ginger are mainly gingerol and zingerone. Siddaraju et al[55] found that an aqueous extract of ginger can protect the gastric mucosa from stress-induced mucosal lesions and inhibit gastric acid secretion, which can be done by blocking H+, K+-ATPase action, thus restricting H. pylori growth. Ginger produces anti-oxidant protection against oxidative stress-induced gastric damage, thus, exhibiting anti-oxidative properties in vitro. Li et al[56] validated and strengthened the association between hyperemesis gravidarum (HG) and H. pylori infection in normal pregnant control subjects and pregnant women with HG. They found positive H. pylori in 1289 (69.6%) HG cases and 1045 (46.2%) H. pylori-positive in the control group. The infection rate of H. pylori was considerably higher in pregnant women with HG compared to the non-HG normal pregnant controls. Analysis of a subgroup revealed that H. pylori infection was a risk factor of HG in other countries, i.e., Oceania, Asia and especially Africa. Karaca et al[57] stated that lower socio-economic status was an important risk factor for H. pylori infected pregnant women with an HG factor. Other studies have found that certain agents active against H. pylori are very effective in the treatment of hyperemesis[58,59]. The human Chorionic Gonadotropin (hCG) when elevated in pregnancy, concurrently alters the pH in pregnancy. hCG was found to induce gastrointestinal dysmotility, altered humoral as well as cell mediated immunity in pregnancy believed to be the basis for infection. Several preclinical studies suggest that ginger, an agent linked to gastric and colon carcinogenesis, generates a protective effect against H. pylori[57,58]. Ginger phenolic fractions provide inhibitory effects on the growth of H. pylori, scavenge free radicals, reduce power abilities, protect DNA and inhibit lipid peroxidation[59,60]. Mahady et al[58] reported on the chemo-preventative effects of ginger which directly impede H. pylori growth, particularly CagA+ strains. The authors showed that gingerols and ginger extracts inhibit the development of H. pylori in vitro of 19 clinical strains. In addition, the fraction comprising the gingerols and 6-shogoal was very successful in inhibiting the growth of H. pylori CagA+ strains. This documentation suggests that specific ginger extracts containing gingerols may assist in treating or preventing H. pylori CagA and strains in vivo. Researchers studying Mongolian gerbils noted that ginger extract prevented and treated H. pylori-induced infection and inflammation[61]. Moreover, additional research was implemented to clarify the in vitro mechanism of the ginger extract. These results confirm the medicinal properties of ginger in Ayurveda and folklore medicines and further advocate that ginger be considered a new therapeutic approach in the treatment of gastric disorders. PISTACIA GUM A resin called Chios mastic gum (CMG), produced by the Pistacia lentiscus var. chia. plant, is nurtured predominantly in the southern part of the Greek island of Chios and other Mediterranean countries. However, this plant can be planted or re-planted in other locations around the world, including the northern part of Chios, however, it will not produce resin. The first mention of mastic was noted by Herodotus in the 5th century BC. Since 3000 BC, CMG has been used by the Greeks in cooking, cosmetics, and treating gastric illnesses. In the 1980s, CMG was found to be a potential agent in treating duodenal ulcers in humans[62]. The antibacterial action of CMG was assessed and compared to clinical isolates of H. pylori[63]. Transmission electron microscopy determined CMG’s influence on H. pylori morphology. CMG presents with anti-H. pylori activity due its inducement of protrusions, morphological abnormalities and cellular fragmentation in H. pylori cells[64]. A 2011 study presented proof that CMG prevents H. pylori inflammation by inhibiting neutrophil activation in vitro[65]. Dabos et al[66] confirmed these observations by examining the influence of CMG on H. pylori eradication in H. pylori patients. Mastic gum was well tolerated and the mild side effects were reversible. It was determined that CMG has bactericidal action against H. pylori in vivo[66]. Paraschos et al[67] found that extracts and elements of CMG were active against H. pylori. After the insoluble polymer was removed, a total mastic extract without polymer was prepared, thus improving solubility and enhancing in vivo activity. The acid fraction generated major triterpenic acids after chromatographic separation, while the neutral fraction generated several triterpenic alcohols and aldehydes. Employing a panel of 11 H. pylori clinical strains, CMG extracts and isolated pure triterpenic acids were tested for in vitro action. The authors demonstrated that administration of CMG may reduce H. pylori settlement. In addition, the major triterpenic acids found in the acid extract may be responsible for this activity[68]. Other animal studies reported that CMG has no effect on H. pylori[68,69]. Monotherapy of CMG was administered to prove its ability to eliminate H. pylori infection in mice. The results showed that CMG was unable to eradicate H. pylori infection in mice. Also, Loughlin et al[69] reported that CMG failed to suppress or destroy H. pylori infection in humans. Patients with H. pylori infection were treated with 1g of CMG, 4 times daily for 14 d. CMG was found to have no effect on H. pylori status; they all remained H. pylori-positive. It was resolved that despite the anti-H. pylori action in vitro, there seems to be no effect on H. pylori in humans due to CMG[69]. All H. pylori-positive patients, treated with mastic capsules for 7 d remained H. pylori positive[70]. Miyamoto et al[70] and Huwez et al[71] observed that no “antibiotic-like” activity should be anticipated from crude mastic. It has been shown that mastic has definite antibacterial action via H. pylori. This may partially explain the anti-peptic-ulcer mastic’s properties[62,71]. By examining the effect of anti-H. pylori of the various elements of mastic, researchers may in the future, identify the participating ingredient. Mastic is inexpensive and widely accessible in third world countries, hence, more in-vivo studies should be performed in developing countries. CONCLUSION Compared with the use of antibiotic and PPI treatment, a preventive dietary approach can be very inexpensive in areas with poor health care systems. The food reviewed can be effective in preventing and/or reducing H. pylori infection due to their potent anti-inflammatory activity. The rapid uptake by cells (Table 1) provides the suggested anti-H. pylori mechanisms of the foods and plant extracts. Table 1 Suggested anti-Helicobacter pylori mechanisms of the foods and plant extracts. Agentadministered Major mechanisms Ref. Cranberry Bacteriostatic properties of proanthocyanidins Howell[8], Gotteland et al[17] Inhibition of adhesion to the human gastric mucosa in vitro Burger et al[9], Parente et al[10], Burger et al[19] Inhibition of adhesion and biofilm formation blocking Shmuely et al[14] Anti-oxidative and anti-carcinogen activity Côté et al[15] Proliferation suppression Matsushima et al[16], Gotteland et al[17] Urease inhibition Lin et al[18] Cytotoxic effect Zafra-Stone et al[20] Garlic Antibacterial activity by thiosulphinates Farbman et al[25] Curcumin Suppression of Matrix Metalloproteinase-3 and -9 expression in H. pylori infected human gastric epithelial cells Kundu et al[45] Inhibition of the shikimate pathway, necessary for synthesis of aromatic amino acids Han et al[46] Effect upon the production of IL-8, IL-1β, tumor necrosis factor-α and cyclooxygenase-2 in gastric mucosa Koosirirat et al[49] Ginger Anti-oxidant and anti-ulcer activity Yoshikawa et al[52] Anti-inﬂammatory and anti-tumor activity Kim et al[53] Blocking H+, K+-ATPase action, inhibitory effects on the growth of H. pylori, DNA protection and inhibition of lipid peroxidation Siddaraju et al[55] 6-gingerol enhances the tumor necrosis factor-related apoptosis by inhibiting nuclear factor kappa B Ishiguro et al[60] Directly inhibiting the growth of H. pylori, particularly the CagA+ strains Mahady et al[58] Pistacia Gum Induction of protrusions, morphological abnormalities, and cellular fragmentation in H. pylori cells Marone et al[64] Inhibition of neutrophil activation Choli-Papadopoulou et al[65] Triterpenic acids present in the acid extract Paraschos et al[67] H. pylori: Helicobacter pylori; IL: Interleukin. Footnotes P- Reviewer: Ierardi E, Ozen H S- Editor: Gong ZM L- Editor: A E- Editor: Wu HL References 1. Covacci A , Telford JL, Del Giudice G, Parsonnet J, Rappuoli R. Helicobacter pylori virulence and genetic geography. Science . 1999; 284 :1328-1333. [ PubMed ] [ DOI ] [ Cited in This Article: ] [ Cited by in Crossref: 787 ] [ Cited by in F6Publishing: 833 ] [ Article Influence: 32.8 ] [ Reference Citation Analysis (0) ] 2. Westblom TU , Czinn SJ, Nedrud JG. Current topics in microbiology and immunology, Gastroduodenal disease and Helicobacter pylori: pathophysiology, diagnosis and treatment . Berlin Heidelberg: Springer 1999; 57-69. [ DOI ] [ Cited in This Article: ] [ Cited by in Crossref: 8 ] [ Article Influence: 0.3 ] [ Reference Citation Analysis (0) ] 3. Kundu P , Mukhopadhyay AK, Patra R, Banerjee A, Berg DE, Swarnakar S. Cag pathogenicity island-independent up-regulation of matrix metalloproteinases-9 and -2 secretion and expression in mice by Helicobacter pylori infection. J Biol Chem . 2006; 281 :34651-34662. [ PubMed ] [ DOI ] [ Cited in This Article: ] [ Cited by in Crossref: 57 ] [ Cited by in F6Publishing: 60 ] [ Article Influence: 3.4 ] [ Reference Citation Analysis (0) ] 4. Graham DY . Efficient identification and evaluation of effective Helicobacter pylori therapies. Clin Gastroenterol Hepatol . 2009; 7 :145-148. [ PubMed ] [ DOI ] [ Cited in This Article: ] [ Cited by in Crossref: 79 ] [ Cited by in F6Publishing: 57 ] [ Article Influence: 5.6 ] [ Reference Citation Analysis (0) ] 5. Mégraud F , Lehours P. Helicobacter pylori detection and antimicrobial susceptibility testing. Clin Microbiol Rev . 2007; 20 :280-322. [ PubMed ] [ DOI ] [ Cited in This Article: ] [ Cited by in Crossref: 425 ] [ Cited by in F6Publishing: 477 ] [ Article Influence: 26.6 ] [ Reference Citation Analysis (0) ] 6. Peterson WL , Graham DY, Marshall B, Blaser MJ, Genta RM, Klein PD, Stratton CW, Drnec J, Prokocimer P, Siepman N. Clarithromycin as monotherapy for eradication of Helicobacter pylori: a randomized, double-blind trial. Am J Gastroenterol . 1993; 88 :1860-1864. [ PubMed ] [ Cited in This Article: ] 7. Calvet X , Gisbert JP, Suarez D. Key points for designing and reporting Helicobacter pylori therapeutic trials: a personal view. Helicobacter . 2011; 16 :346-355. [ PubMed ] [ DOI ] [ Cited in This Article: ] [ Cited by in Crossref: 10 ] [ Cited by in F6Publishing: 8 ] [ Article Influence: 0.8 ] [ Reference Citation Analysis (0) ] 8. Howell AB . Cranberry proanthocyanidins and the maintenance of urinary tract health. Crit Rev Food Sci Nutr . 2002; 42 :273-278. [ PubMed ] [ DOI ] [ Cited in This Article: ] [ Cited by in Crossref: 99 ] [ Cited by in F6Publishing: 77 ] [ Article Influence: 4.7 ] [ Reference Citation Analysis (0) ] 9. Burger O , Ofek I, Tabak M, Weiss EI, Sharon N, Neeman I. A high molecular mass constituent of cranberry juice inhibits helicobacter pylori adhesion to human gastric mucus. FEMS Immunol Med Microbiol . 2000; 29 :295-301. [ PubMed ] [ DOI ] [ Cited in This Article: ] [ Cited by in Crossref: 149 ] [ Cited by in F6Publishing: 127 ] [ Article Influence: 6.8 ] [ Reference Citation Analysis (0) ] 10. Parente F , Cucino C, Anderloni A, Grandinetti G, Bianchi Porro G. Treatment of Helicobacter pylori infection using a novel antiadhesion compound (3’sialyllactose sodium salt). A double blind, placebo-controlled clinical study. Helicobacter . 2003; 8 :252-256. [ PubMed ] [ DOI ] [ Cited in This Article: ] [ Cited by in Crossref: 39 ] [ Cited by in F6Publishing: 39 ] [ Article Influence: 2.0 ] [ Reference Citation Analysis (0) ] 11. Ilver D , Arnqvist A, Ogren J, Frick IM, Kersulyte D, Incecik ET, Berg DE, Covacci A, Engstrand L, Borén T. Helicobacter pylori adhesin binding fucosylated histo-blood group antigens revealed by retagging. Science . 1998; 279 :373-377. [ PubMed ] [ DOI ] [ Cited in This Article: ] [ Cited by in Crossref: 872 ] [ Cited by in F6Publishing: 933 ] [ Article Influence: 34.9 ] [ Reference Citation Analysis (1) ] 12. Guruge JL , Falk PG, Lorenz RG, Dans M, Wirth HP, Blaser MJ, Berg DE, Gordon JI. Epithelial attachment alters the outcome of Helicobacter pylori infection. Proc Natl Acad Sci USA . 1998; 95 :3925-3930. [ PubMed ] [ Cited in This Article: ] 13. Xiao SD , Shi T. Is cranberry juice effective in the treatment and prevention of Helicobacter pylori infection in mice? Chinese J Dig Dis . 2003; 4 :136-139. [ DOI ] [ Cited in This Article: ] [ Cited by in Crossref: 17 ] [ Cited by in F6Publishing: 17 ] [ Article Influence: 0.9 ] [ Reference Citation Analysis (0) ] 14. Shmuely H , Ofek I, Weiss EI, Rones Z, Houri-Haddad Y. Cranberry components for the therapy of infectious disease. Curr Opin Biotechnol . 2012; 23 :148-152. [ PubMed ] [ DOI ] [ Cited in This Article: ] [ Cited by in Crossref: 36 ] [ Cited by in F6Publishing: 38 ] [ Article Influence: 3.0 ] [ Reference Citation Analysis (0) ] 15. Côté J , Caillet S, Doyon G, Sylvain JF, Lacroix M. Bioactive compounds in cranberries and their biological properties. Crit Rev Food Sci Nutr . 2010; 50 :666-679. [ PubMed ] [ DOI ] [ Cited in This Article: ] [ Cited by in Crossref: 152 ] [ Cited by in F6Publishing: 123 ] [ Article Influence: 11.7 ] [ Reference Citation Analysis (0) ] 16. Matsushima M , Suzuki T, Masui A, Kasai K, Kouchi T, Takagi A, Shirai T, Mine T. Growth inhibitory action of cranberry on Helicobacter pylori. J Gastroenterol Hepatol . 2008; 23 Suppl 2 :S175-S180. [ PubMed ] [ DOI ] [ Cited in This Article: ] [ Cited by in Crossref: 28 ] [ Cited by in F6Publishing: 33 ] [ Article Influence: 1.9 ] [ Reference Citation Analysis (0) ] 17. Gotteland M , Andrews M, Toledo M, Muñoz L, Caceres P, Anziani A, Wittig E, Speisky H, Salazar G. Modulation of Helicobacter pylori colonization with cranberry juice and Lactobacillus johnsonii La1 in children. Nutrition . 2008; 24 :421-426. [ PubMed ] [ DOI ] [ Cited in This Article: ] [ Cited by in Crossref: 98 ] [ Cited by in F6Publishing: 102 ] [ Article Influence: 6.5 ] [ Reference Citation Analysis (0) ] 18. Lin YT , Kwon YI, Labbe RG, Shetty K. Inhibition of Helicobacter pylori and associated urease by oregano and cranberry phytochemical synergies. Appl Environ Microbiol . 2005; 71 :8558-8564. [ PubMed ] [ DOI ] [ Cited in This Article: ] [ Cited by in Crossref: 105 ] [ Cited by in F6Publishing: 108 ] [ Article Influence: 6.2 ] [ Reference Citation Analysis (0) ] 19. Burger O , Weiss E, Sharon N, Tabak M, Neeman I, Ofek I. Inhibition of Helicobacter pylori adhesion to human gastric mucus by a high-molecular-weight constituent of cranberry juice. Crit Rev Food Sci Nutr . 2002; 42 :279-284. [ PubMed ] [ DOI ] [ Cited in This Article: ] [ Cited by in Crossref: 96 ] [ Cited by in F6Publishing: 73 ] [ Article Influence: 4.6 ] [ Reference Citation Analysis (0) ] 20. Zafra-Stone S , Yasmin T, Bagchi M, Chatterjee A, Vinson JA, Bagchi D. Berry anthocyanins as novel antioxidants in human health and disease prevention. Mol Nutr Food Res . 2007; 51 :675-683. [ PubMed ] [ DOI ] [ Cited in This Article: ] [ Cited by in Crossref: 622 ] [ Cited by in F6Publishing: 633 ] [ Article Influence: 38.9 ] [ Reference Citation Analysis (0) ] 21. Chatterjee A , Yasmin T, Bagchi D, Stohs SJ. Inhibition of Helicobacter pylori in vitro by various berry extracts, with enhanced susceptibility to clarithromycin. Mol Cell Biochem . 2004; 265 :19-26. [ PubMed ] [ DOI ] [ Cited in This Article: ] [ Cited by in Crossref: 72 ] [ Cited by in F6Publishing: 75 ] [ Article Influence: 4.0 ] [ Reference Citation Analysis (0) ] 22. Shmuely H , Burger O, Neeman I, Yahav J, Samra Z, Niv Y, Sharon N, Weiss E, Athamna A, Tabak M. Susceptibility of Helicobacter pylori isolates to the antiadhesion activity of a high-molecular-weight constituent of cranberry. Diagn Microbiol Infect Dis . 2004; 50 :231-235. [ PubMed ] [ DOI ] [ Cited in This Article: ] [ Cited by in Crossref: 64 ] [ Cited by in F6Publishing: 65 ] [ Article Influence: 3.6 ] [ Reference Citation Analysis (0) ] 23. Zhang L , Ma J, Pan K, Go VL, Chen J, You WC. Efficacy of cranberry juice on Helicobacter pylori infection: a double-blind, randomized placebo-controlled trial. Helicobacter . 2005; 10 :139-145. [ PubMed ] [ DOI ] [ Cited in This Article: ] [ Cited by in F6Publishing: 1 ] [ Reference Citation Analysis (0) ] 24. Shmuely H , Yahav J, Samra Z, Chodick G, Koren R, Niv Y, Ofek I. Effect of cranberry juice on eradication of Helicobacter pylori in patients treated with antibiotics and a proton pump inhibitor. Mol Nutr Food Res . 2007; 51 :746-751. [ PubMed ] [ DOI ] [ Cited in This Article: ] [ Cited by in Crossref: 51 ] [ Cited by in F6Publishing: 54 ] [ Article Influence: 3.2 ] [ Reference Citation Analysis (0) ] 25. Farbman KS , Barnett ED, Bolduc GR, Klein JO. Antibacterial activity of garlic and onions: a historical perspective. Pediatr Infect Dis J . 1993; 12 :613-614. [ PubMed ] [ DOI ] [ Cited in This Article: ] [ Cited by in Crossref: 42 ] [ Cited by in F6Publishing: 42 ] [ Article Influence: 1.4 ] [ Reference Citation Analysis (0) ] 26. Cañizares P , Gracia I, Gómez LA, Martín de Argila C, de Rafael L, García A. Optimization of Allium sativum solvent extraction for the inhibition of in vitro growth of Helicobacter pylori. Biotechnol Prog . 2002; 18 :1227-1232. [ PubMed ] [ DOI ] [ Cited in This Article: ] [ Cited by in Crossref: 23 ] [ Cited by in F6Publishing: 24 ] [ Article Influence: 1.1 ] [ Reference Citation Analysis (0) ] 27. Lawson LD , Wang ZJ, Papadimitriou D. Allicin release under simulated gastrointestinal conditions from garlic powder tablets employed in clinical trials on serum cholesterol. Planta Med . 2001; 67 :13-18. [ PubMed ] [ DOI ] [ Cited in This Article: ] [ Cited by in Crossref: 43 ] [ Cited by in F6Publishing: 34 ] [ Article Influence: 2.0 ] [ Reference Citation Analysis (0) ] 28. Cañizares P , Gracia I, Gómez LA, García A, Martín De Argila C, Boixeda D, de Rafael L. Thermal degradation of allicin in garlic extracts and its implication on the inhibition of the in-vitro growth of Helicobacter pylori. Biotechnol Prog . 2004; 20 :32-37. [ PubMed ] [ DOI ] [ Cited in This Article: ] [ Cited by in Crossref: 55 ] [ Cited by in F6Publishing: 55 ] [ Article Influence: 2.9 ] [ Reference Citation Analysis (0) ] 29. Dorant E , van den Brandt PA, Goldbohm RA, Sturmans F. Consumption of onions and a reduced risk of stomach carcinoma. Gastroenterology . 1996; 110 :12-20. [ PubMed ] [ DOI ] [ Cited in This Article: ] [ Cited by in Crossref: 154 ] [ Cited by in F6Publishing: 156 ] [ Article Influence: 5.7 ] [ Reference Citation Analysis (0) ] 30. You WC , Brown LM, Zhang L, Li JY, Jin ML, Chang YS, Ma JL, Pan KF, Liu WD, Hu Y. Randomized double-blind factorial trial of three treatments to reduce the prevalence of precancerous gastric lesions. J Natl Cancer Inst . 2006; 98 :974-983. [ PubMed ] [ DOI ] [ Cited in This Article: ] [ Cited by in Crossref: 310 ] [ Cited by in F6Publishing: 329 ] [ Article Influence: 18.2 ] [ Reference Citation Analysis (0) ] 31. Tang HR , Fan YJ, Liu S. Helicobacter pylori infection and associated risk factors in Chengdu. Sichuan Daxue Xuebao Yixueban . 2014; 45 :823-826. [ PubMed ] [ Cited in This Article: ] 32. Salih BA , Abasiyanik FM. Does regular garlic intake affect the prevalence of Helicobacter pylori in asymptomatic subjects? Saudi Med J . 2003; 24 :842-845. [ PubMed ] [ Cited in This Article: ] 33. McNulty CA , Wilson MP, Havinga W, Johnston B, O’Gara EA, Maslin DJ. A pilot study to determine the effectiveness of garlic oil capsules in the treatment of dyspeptic patients with Helicobacter pylori. Helicobacter . 2001; 6 :249-253. [ PubMed ] [ DOI ] [ Cited in This Article: ] [ Cited by in Crossref: 28 ] [ Cited by in F6Publishing: 26 ] [ Article Influence: 1.3 ] [ Reference Citation Analysis (1) ] 34. Aydin A , Ersöz G, Tekesin O, Akçiçek E, Tuncyurek M, Batur Y. Does garlic oil have a role in the treatment of Helicobacter pylori infection? Turk Gastroenteroloji Dergisi . 1997; 8 :181-184. [ Cited in This Article: ] 35. Sharma RA , Gescher AJ, Steward WP. Curcumin: the story so far. Eur J Cancer . 2005; 41 :1955-1968. [ PubMed ] [ DOI ] [ Cited in This Article: ] [ Cited by in Crossref: 1124 ] [ Cited by in F6Publishing: 1168 ] [ Article Influence: 62.4 ] [ Reference Citation Analysis (0) ] 36. Egan ME , Pearson M, Weiner SA, Rajendran V, Rubin D, Glöckner-Pagel J, Canny S, Du K, Lukacs GL, Caplan MJ. Curcumin, a major constituent of turmeric, corrects cystic fibrosis defects. Science . 2004; 304 :600-602. [ PubMed ] [ DOI ] [ Cited in This Article: ] [ Cited by in Crossref: 414 ] [ Cited by in F6Publishing: 439 ] [ Article Influence: 21.8 ] [ Reference Citation Analysis (0) ] 37. Bengmark S . Curcumin, an atoxic antioxidant and natural NFkappaB, cyclooxygenase-2, lipooxygenase, and inducible nitric oxide synthase inhibitor: a shield against acute and chronic diseases. JPEN J Parenter Enteral Nutr . 2006; 30 :45-51. [ PubMed ] [ DOI ] [ Cited in This Article: ] [ Cited by in Crossref: 230 ] [ Cited by in F6Publishing: 248 ] [ Article Influence: 13.5 ] [ Reference Citation Analysis (0) ] 38. Punithavathi D , Venkatesan N, Babu M. Protective effects of curcumin against amiodarone-induced pulmonary fibrosis in rats. Br J Pharmacol . 2003; 139 :1342-1350. [ PubMed ] [ DOI ] [ Cited in This Article: ] [ Cited by in Crossref: 75 ] [ Cited by in F6Publishing: 77 ] [ Article Influence: 3.9 ] [ Reference Citation Analysis (0) ] 39. Ringman JM , Frautschy SA, Cole GM, Masterman DL, Cummings JL. A potential role of the curry spice curcumin in Alzheimer’s disease. Curr Alzheimer Res . 2005; 2 :131-136. [ PubMed ] [ DOI ] [ Cited in This Article: ] [ Cited by in Crossref: 335 ] [ Cited by in F6Publishing: 362 ] [ Article Influence: 19.7 ] [ Reference Citation Analysis (0) ] 40. Duvoix A , Blasius R, Delhalle S, Schnekenburger M, Morceau F, Henry E, Dicato M, Diederich M. Chemopreventive and therapeutic effects of curcumin. Cancer Lett . 2005; 223 :181-190. [ PubMed ] [ DOI ] [ Cited in This Article: ] [ Cited by in Crossref: 593 ] [ Cited by in F6Publishing: 616 ] [ Article Influence: 32.9 ] [ Reference Citation Analysis (0) ] 41. Holt PR , Katz S, Kirshoff R. Curcumin therapy in inflammatory bowel disease: a pilot study. Dig Dis Sci . 2005; 50 :2191-2193. [ PubMed ] [ DOI ] [ Cited in This Article: ] [ Cited by in Crossref: 274 ] [ Cited by in F6Publishing: 270 ] [ Article Influence: 15.2 ] [ Reference Citation Analysis (0) ] 42. Swarnakar S , Ganguly K, Kundu P, Banerjee A, Maity P, Sharma AV. Curcumin regulates expression and activity of matrix metalloproteinases 9 and 2 during prevention and healing of indomethacin-induced gastric ulcer. J Biol Chem . 2005; 280 :9409-9415. [ PubMed ] [ DOI ] [ Cited in This Article: ] [ Cited by in Crossref: 165 ] [ Cited by in F6Publishing: 170 ] [ Article Influence: 8.7 ] [ Reference Citation Analysis (0) ] 43. Foryst-Ludwig A , Neumann M, Schneider-Brachert W, Naumann M. Curcumin blocks NF-kappaB and the motogenic response in Helicobacter pylori-infected epithelial cells. Biochem Biophys Res Commun . 2004; 316 :1065-1072. [ PubMed ] [ Cited in This Article: ] 44. Santos AM , Lopes T, Oleastro M, Gato IV, Floch P, Benejat L, Chaves P, Pereira T, Seixas E, Machado J. Curcumin inhibits gastric inflammation induced by Helicobacter pylori infection in a mouse model. Nutrients . 2015; 7 :306-320. [ PubMed ] [ DOI ] [ Cited in This Article: ] [ Cited by in Crossref: 40 ] [ Cited by in F6Publishing: 45 ] [ Article Influence: 5.0 ] [ Reference Citation Analysis (0) ] 45. Kundu P , De R, Pal I, Mukhopadhyay AK, Saha DR, Swarnakar S. Curcumin alleviates matrix metalloproteinase-3 and -9 activities during eradication of Helicobacter pylori infection in cultured cells and mice. PLoS One . 2011; 6 :e16306. [ PubMed ] [ DOI ] [ Cited in This Article: ] [ Cited by in Crossref: 51 ] [ Cited by in F6Publishing: 58 ] [ Article Influence: 4.3 ] [ Reference Citation Analysis (0) ] 46. Han C , Wang L, Yu K, Chen L, Hu L, Chen K, Jiang H, Shen X. Biochemical characterization and inhibitor discovery of shikimate dehydrogenase from Helicobacter pylori. FEBS J . 2006; 273 :4682-4692. [ PubMed ] [ Cited in This Article: ] 47. Cheng WC , Chen YF, Wang HJ, Hsu KC, Lin SC, Chen TJ, Yang JM, Wang WC. Structures of Helicobacter pylori shikimate kinase reveal a selective inhibitor-induced-fit mechanism. PLoS One . 2012; 7 :e33481. [ PubMed ] [ DOI ] [ Cited in This Article: ] [ Cited by in Crossref: 22 ] [ Cited by in F6Publishing: 22 ] [ Article Influence: 2.0 ] [ Reference Citation Analysis (0) ] 48. Coggins JR , Abell C, Evans LB, Frederickson M, Robinson DA, Roszak AW, Lapthorn AP. Experiences with the shikimate-pathway enzymes as targets for rational drug design. Biochem Soc Trans . 2003; 31 :548-552. [ PubMed ] [ Cited in This Article: ] 49. Koosirirat C , Linpisarn S, Changsom D, Chawansuntati K, Wipasa J. Investigation of the anti-inflammatory effect of Curcuma longa in Helicobacter pylori-infected patients. Int Immunopharmacol . 2010; 10 :815-818. [ PubMed ] [ DOI ] [ Cited in This Article: ] [ Cited by in Crossref: 72 ] [ Cited by in F6Publishing: 56 ] [ Article Influence: 5.5 ] [ Reference Citation Analysis (0) ] 50. Prucksunand C , Indrasukhsri B, Leethochawalit M, Hungspreugs K. Phase II clinical trial on effect of the long turmeric (Curcuma longa Linn) on healing of peptic ulcer. Southeast Asian J Trop Med Public Health . 2001; 32 :208-215. [ PubMed ] [ Cited in This Article: ] 51. Farnsworth RF , Fong HHS, Mahady GB. WHO monographs on selected medicinal plants . Geneva, Switzerland: WHO Publications 1999; . [ Cited in This Article: ] 52. Yoshikawa M , Yamaguchi S, Kunimi K, Matsuda H, Okuno Y, Yamahara J, Murakami N. Stomachic principles in ginger. III. An anti-ulcer principle, 6-gingesulfonic acid, and three monoacyldigalactosylglycerols, gingerglycolipids A, B, and C, from Zingiberis Rhizoma originating in Taiwan. Chem Pharm Bull (Tokyo) . 1994; 42 :1226-1230. [ PubMed ] [ DOI ] [ Cited in This Article: ] [ Cited by in Crossref: 90 ] [ Cited by in F6Publishing: 93 ] [ Article Influence: 3.1 ] [ Reference Citation Analysis (0) ] 53. Kim EC , Min JK, Kim TY, Lee SJ, Yang HO, Han S, Kim YM, Kwon YG. [6]-Gingerol, a pungent ingredient of ginger, inhibits angiogenesis in vitro and in vivo. Biochem Biophys Res Commun . 2005; 335 :300-308. [ PubMed ] [ DOI ] [ Cited in This Article: ] [ Cited by in Crossref: 182 ] [ Cited by in F6Publishing: 184 ] [ Article Influence: 10.1 ] [ Reference Citation Analysis (0) ] 54. al-Yahya MA , Rafatullah S, Mossa JS, Ageel AM, Parmar NS, Tariq M. Gastroprotective activity of ginger zingiber officinale rosc., in albino rats. Am J Chin Med . 1989; 17 :51-56. [ PubMed ] [ DOI ] [ Cited in This Article: ] [ Cited by in Crossref: 68 ] [ Cited by in F6Publishing: 73 ] [ Article Influence: 2.0 ] [ Reference Citation Analysis (0) ] 55. Siddaraju MN , Dharmesh SM. Inhibition of gastric H+, K+-ATPase and Helicobacter pylori growth by phenolic antioxidants of Zingiber officinale. Mol Nutr Food Res . 2007; 51 :324-332. [ PubMed ] [ DOI ] [ Cited in This Article: ] [ Cited by in Crossref: 62 ] [ Cited by in F6Publishing: 66 ] [ Article Influence: 3.9 ] [ Reference Citation Analysis (0) ] 56. Li L , Li L, Zhou X, Xiao S, Gu H, Zhang G. Helicobacter pylori Infection Is Associated with an Increased Risk of Hyperemesis Gravidarum: A Meta-Analysis. Gastroenterol Res Pract . 2015; 2015 :278905. [ PubMed ] [ DOI ] [ Cited in This Article: ] [ Cited by in Crossref: 24 ] [ Cited by in F6Publishing: 28 ] [ Article Influence: 3.0 ] [ Reference Citation Analysis (0) ] 57. Karaca C , Güler N, Yazar A, Camlica H, Demir K, Yildirim G. Is lower socio-economic status a risk factor for Helicobacter pylori infection in pregnant women with hyperemesis gravidarum? Turk J Gastroenterol . 2004; 15 :86-89. [ PubMed ] [ Cited in This Article: ] 58. Mahady GB , Pendland SL, Yun GS, Lu ZZ, Stoia A. Ginger (Zingiber officinale Roscoe) and the gingerols inhibit the growth of Cag A+ strains of Helicobacter pylori. Anticancer Res . 2003; 23 :3699-3702. [ PubMed ] [ Cited in This Article: ] 59. El Younis CM , Abulafia O, Sherer DM. Rapid marked response of severe hyperemesis gravidarum to oral erythromycin. Am J Perinatol . 1998; 15 :533-534. [ PubMed ] [ DOI ] [ Cited in This Article: ] [ Cited by in Crossref: 20 ] [ Cited by in F6Publishing: 19 ] [ Article Influence: 0.8 ] [ Reference Citation Analysis (0) ] 60. Ishiguro K , Ando T, Maeda O, Ohmiya N, Niwa Y, Kadomatsu K, Goto H. Ginger ingredients reduce viability of gastric cancer cells via distinct mechanisms. Biochem Biophys Res Commun . 2007; 362 :218-223. [ PubMed ] [ Cited in This Article: ] 61. Gaus K , Huang Y, Israel DA, Pendland SL, Adeniyi BA, Mahady GB. Standardized ginger (Zingiber officinale) extract reduces bacterial load and suppresses acute and chronic inflammation in Mongolian gerbils infected with cagAHelicobacter pylori. Pharm Biol . 2009; 47 :92-98. [ PubMed ] [ DOI ] [ Cited in This Article: ] [ Cited by in Crossref: 71 ] [ Cited by in F6Publishing: 78 ] [ Article Influence: 1.8 ] [ Reference Citation Analysis (0) ] 62. Al-Habbal MJ , Al-Habbal Z, Huwez FU. A double-blind controlled clinical trial of mastic and placebo in the treatment of duodenal ulcer. Clin Exp Pharmacol Physiol . 1984; 11 :541-544. [ PubMed ] [ Cited in This Article: ] 63. Aebischer T , Meyer TF, Andersen LP. Inflammation, immunity, and vaccines for Helicobacter. Helicobacter . 2010; 15 Suppl 1 :21-28. [ PubMed ] [ DOI ] [ Cited in This Article: ] [ Cited by in Crossref: 22 ] [ Cited by in F6Publishing: 24 ] [ Article Influence: 1.7 ] [ Reference Citation Analysis (0) ] 64. Marone P , Bono L, Leone E, Bona S, Carretto E, Perversi L. Bactericidal activity of Pistacia lentiscus mastic gum against Helicobacter pylori. J Chemother . 2001; 13 :611-614. [ PubMed ] [ Cited in This Article: ] 65. Choli-Papadopoulou T , Kottakis F, Papadopoulos G, Pendas S. Helicobacter pylori neutrophil activating protein as target for new drugs against H. pylori inflammation. World J Gastroenterol . 2011; 17 :2585-2591. [ PubMed ] [ DOI ] [ Cited in This Article: ] [ Cited by in CrossRef: 9 ] [ Cited by in F6Publishing: 11 ] [ Article Influence: 0.8 ] [ Reference Citation Analysis (0) ] 66. Dabos KJ , Sfika E, Vlatta LJ, Giannikopoulos G. The effect of mastic gum on Helicobacter pylori: a randomized pilot study. Phytomedicine . 2010; 17 :296-299. [ PubMed ] [ DOI ] [ Cited in This Article: ] [ Cited by in Crossref: 45 ] [ Cited by in F6Publishing: 47 ] [ Article Influence: 3.2 ] [ Reference Citation Analysis (0) ] 67. Paraschos S , Magiatis P, Mitakou S, Petraki K, Kalliaropoulos A, Maragkoudakis P, Mentis A, Sgouras D, Skaltsounis AL. In vitro and in vivo activities of Chios mastic gum extracts and constituents against Helicobacter pylori. Antimicrob Agents Chemother . 2007; 51 :551-559. [ PubMed ] [ Cited in This Article: ] 68. Bebb JR , Bailey-Flitter N, Ala’Aldeen D, Atherton JC. Mastic gum has no effect on Helicobacter pylori load in vivo. J Antimicrob Chemother . 2003; 52 :522-523. [ PubMed ] [ Cited in This Article: ] 69. Loughlin MF , Ala’Aldeen DA, Jenks PJ. Monotherapy with mastic does not eradicate Helicobacter pylori infection from mice. J Antimicrob Chemother . 2003; 51 :367-371. [ PubMed ] [ Cited in This Article: ] 70. Miyamoto T , Okimoto T, Kuwano M. Chemical Composition of the Essential Oil of Mastic Gum and their Antibacterial Activity Against Drug-Resistant Helicobacter pylori. Nat Prod Bioprospect . 2014; 4 :227-231. [ PubMed ] [ DOI ] [ Cited in This Article: ] [ Cited by in Crossref: 31 ] [ Cited by in F6Publishing: 33 ] [ Article Influence: 3.4 ] [ Reference Citation Analysis (0) ] 71. Huwez FU , Al-Habbal MJ. Mastic in treatment of benign gastric ulcers. Gastroenterol Jpn . 1986; 21 :273-274. 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