The green tea polyphenol epigallocatechin-3-gallate effectively inhibits Helicobacter pylori-induced gastritis in Mongolian gerbils

被引:0
作者
Jiang, Jing [1 ]
Cao, Donghui [1 ]
Jia, Zhifang [1 ]
You, Lili [1 ]
Tsukamoto, Tetsuya [2 ]
Hou, Zhen [3 ]
Suo, Yueer [3 ]
Wang, Shidong [3 ]
Cao, Xueyuan [3 ]
机构
[1] Jilin Univ, Hosp 1, Div Clin Epidemiol, Changchun 130021, Jilin Province, Peoples R China
[2] Fujita Hlth Univ, Sch Med, Div Pathol 1, Toyoake, Aichi 47011, Japan
[3] Jilin Univ, Hosp 1, Dept Gastr & Colorectal Surg, 71st Xin Min St, Changchun 130021, Jilin Province, Peoples R China
来源
INTERNATIONAL JOURNAL OF CLINICAL AND EXPERIMENTAL MEDICINE | 2016年 / 9卷 / 02期
基金
中国国家自然科学基金;
关键词
Epigallocatechin-3-gallate; Helicobacter pylori; gastritis; inflammation; 4-VINYL-2,6-DIMETHOXYPHENOL CANOLOL; INFECTION; THERAPY; CANCER; CARCINOGENESIS; CLARITHROMYCIN; RESISTANCE;
D O I
暂无
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Background: Epigallocatechin-3-gallate (EGCG) is a major catechin of green tea; it has protective effects against injury and exhibits anti-inflammatory activity. Helicobacter pylori (H. pylori) eradication rates with clarithromycin-based triple therapy are declining, and an alternative strategy is urgently needed. The activity of EGCG against H. pylori-infected gastritis was investigated in an in vivo Mongolian gerbil model. Methods: Mongolian gerbils were randomly divided into H. pylori-infected, H. pylori-infected + drinking water containing 0.05% EGCG, triple treatment (amoxicillin, clarithromycin and esomeprazole), and control groups. After 12 weeks, gastric pH tests and histopathological evaluations were performed, and mucosal interleukin-1 beta (IL-1 beta), tumor necrosis factor-alpha (TNF-alpha), cyclooxygenase-2 (COX-2), and inducible nitric oxide synthase (iNOS) levels in the gastric mucosa were investigated. Results: Significant inflammatory mucosal changes were observed in the H. pylori infection groups. The EGCG and triple-drug treatments significantly decreased the severity of gastritis in the antrum and the corpus. The mRNA levels of IL-1 beta, TNF-alpha, COX-2 and iNOS were increased in the H. pylori-infected gastric mucosa and obviously lower in the EGCG group than in the H. pylori-infection groups. Conclusions: The activations of IL-1 beta, TNF-alpha, COX-2 and iNOS were essential for H. pylori-induced gastritis in Mongolian gerbils. EGCG exhibited anti-inflammatory effects that might be mediated through the inhibitions of IL-1 beta, TNF-alpha, COX-2 and iNOS in the gerbil model of H. pylori-induced inflammation.
引用
收藏
页码:2479 / 2485
页数:7
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