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Dietary Intervention of Artemisia and Green Tea Extracts to Rejuvenate Helicobacter pylori ‐Associated Chronic Atrophic Gastritis and to Prevent Tumorigenesis
Author(s) -
Jeong Migyeong,
Park JongMin,
Han YoungMin,
Kangwan Napapan,
Kwon SangOh,
Kim BokNam,
Kim WonHee,
Hahm KiBaik
Publication year - 2016
Publication title -
helicobacter
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.206
H-Index - 79
eISSN - 1523-5378
pISSN - 1083-4389
DOI - 10.1111/hel.12229
Subject(s) - helicobacter pylori , atrophic gastritis , gastroenterology , medicine , gastritis , lesion , helicobacter , carcinogenesis , stomach , pathology , cancer
Object As nonmicrobial dietary approach is capable of controlling H elicobacter pylori infection, we evaluated the efficacy of long‐term dietary administration of A rtemisia and/or green tea extracts on H . pylori ‐initiated, high‐salt‐promoted chronic atrophic gastritis and gastric tumorigenesis mouse model. Methods Helicobacter pylori ‐infected and high‐salt‐diet‐administered C 57 BL /6 mice were administered with A rtemisia extracts ( MP group) and/or green tea extracts ( GT group) for 36 weeks in addition to the control group ( ES group, gastroprotective drug, ecabet sodium 30 mg/kg, diet pellet). Gross and pathological gastric lesions were evaluated after 24 and 36 weeks, respectively, and their underlying molecular changes were measured in gastric homogenates. Detailed mechanisms were further evaluated in in vitro cell models. Results The erythematous and nodular changes and mucosal ulcerative and erosive lesions were noted in the control group at 24 weeks. MP , GT , MPGT , and ES groups all showed significantly ameliorated pathologic lesion compared to the control group ( p < .05). After the 36 weeks, scattered nodular masses with some central ulcers and thin gastric surface were noted in the control stomach, whereas no tumorous lesion and milder atrophic changes were observed in all MP , GT , and MPGT groups except ES group ( p < .05). On molecular analysis, increased expressions of COX ‐2, TNF ‐α, IL ‐6, lipid peroxide, and activated STAT 3 relevant to H. pylori infection were significantly decreased with MPGT administration ( p < .01), whereas HSP 70 was significantly increased. PGDH expressions, core tumor suppressor involved in carcinogenesis, were significantly decreased with H. pylori infection ( p < .05), but significantly increased in MPGT group ( p < .05). Increased mucosal apoptotic index noted in the control group was significantly decreased with MP and/or GT along with significantly preserved gastric gastroprotective mediators ( p < .01) such as mucins, HSP 27, and HSP 70. H. pylori ‐induced serum TNF ‐α and NF ‐κB activations were significantly decreased with MPGT administration ( p < .05). Conclusion Long‐term dietary intake of MP and/or GT can be an effective strategy either to rejuvenate H. pylori atrophic gastritis or to suppress tumorigenesis.