pylori)-induced gastritis through its anti-oxidative and antibact

pylori)-induced gastritis through its anti-oxidative and antibacterial actions. In this study, we investigated the in vivo activity of EGCG against H. pylori-infected gastritis in Mongolian gerbil animal models, and evaluated the role of inflammatory

cytokines pathway. Methods: Six-week-old gerbils were randomly divided into three groups: H. pylori infected group (n = 10), H. pylori infected + drinking water containg EGCG group (n = 10), and control group (n = 10). The animals were inoculated with H. pylori, drinking water containing 0.05% EGCG, and then sacrificed after 20 weeks. The stomachs were excised, processed routinely, and analyzed histologically. The mRNA levels for mucosal interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), cyclooxygenase-2 (COX-2), and inducible nitric oxide synthase (iNOS) in gastric mucosa were investigated with quantitative RT-PCR. Results: The pathological examination showed significant inflammatory mucosal changes in infection rate was 100% in the H. pylori infection model group. EGCG significantly decreased the severity of gastritis in the antrum and the corpus. At the same time, Relative mRNA expression levels of IL-1β, TNF-α, COX-2 and iNOS LDK378 were significantly increased in H. pylori -infected gastric mucosa[IL-1β (138 vs.1.0), TNF-α (13.7 vs.1.0), COX-2(61.9 vs.1.0)

and iNOS (36.3 vs.1.0), P < 0.001], and obviously inhibited in the EGCG group than those in the control medchemexpress group[IL-1β (37.7 vs.138), TNF-α (4.9 vs.13.7), COX-2(33.1 vs.61.9) and iNOS (15.2 vs.36.3), P < 0.01]. Conclusion: These results suggest that activation of IL-1β, TNF-α, COX-2 and iNOS were essential for H. pylori-induced gastritis in Mongolian gerbils. EGCG exhibits anti-inflammatory effects might through inhibition of IL-1β, TNF-α, COX-2 and iNOS in gerbil model of H. pylori -induced inflammatory. This work was part supported by

National Natural Science Foundation of China, No. 81273065 and No.81072369. Key Word(s): 1. H.pylori; 2. EGCG; 3. inflammation; 4. gerbil; Presenting Author: MICHAEL MOLLOY-BLAND Additional Authors: PETER NAGY, STEPHEN SWEET, SAGA JOHANSSON, TORE LIND Corresponding Author: MICHAEL MOLLOY-BLAND Affiliations: AstraZeneca; Research Evaluation Unit, Oxford PharmaGenesis Ltd. Objective: It has been suggested that the prevalence of Helicobacter pylori infection, a major cause of peptic ulcer disease (PUD), has stabilized in the USA but is decreasing in China. We conducted a systematic literature analysis to test this hypothesis. Methods: PubMed searches were conducted up to July 2012. Trends in the reported prevalence of H. pylori infection over time were assessed by regression analysis using Microsoft Excel. In addition, Chinese and US studies were grouped according to whether their study midpoint was before or after the mean of all study midpoints, and weighted mean prevalence estimates for H.

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