TY - JOUR
T1 - The green tea polyphenol epigallocatechin-3-gallate effectively inhibits helicobacter pylori-induced gastritis in Mongolian gerbils
AU - Jiang, Jing
AU - Cao, Donghui
AU - Jia, Zhifang
AU - You, Lili
AU - Tsukamoto, Tetsuya
AU - Hou, Zhen
AU - Suo, Yueer
AU - Wang, Shidong
AU - Cao, Xueyuan
N1 - Funding Information:
This study was partially supported by the National Natural Science Foundation of China (No. 81273065 and 81373084) and the Norman Bethune Program of Jilin University (No. 2013025)
Publisher Copyright:
© 2016, E-Century Publishing Corporation. All rights reserved.
Copyright:
Copyright 2018 Elsevier B.V., All rights reserved.
PY - 2016/2/29
Y1 - 2016/2/29
N2 - 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-1β (IL-1β), tumor necrosis factor-α (TNF-α), 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-1β, TNF-α, 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-1β, TNF-α, 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-1β, TNF-α, COX-2 and iNOS in the gerbil model of H. pylori-induced inflammation.
AB - 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-1β (IL-1β), tumor necrosis factor-α (TNF-α), 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-1β, TNF-α, 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-1β, TNF-α, 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-1β, TNF-α, COX-2 and iNOS in the gerbil model of H. pylori-induced inflammation.
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M3 - Article
AN - SCOPUS:84962210153
VL - 9
SP - 2479
EP - 2485
JO - International Journal of Clinical and Experimental Medicine
JF - International Journal of Clinical and Experimental Medicine
SN - 1940-5901
IS - 2
ER -