2012•WeichangbingxueRequires access
Effect of Teprenone on p16 and TGF-β1 Expressions in Gastric Mucosa of Rats with Atrophic Gastritis
Wang Huimin
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Abstract
Background: Chronic atrophic gastritis(CAG) is a precancerous lesion of gastric cancer.Therefore,preventing and interrupting the CAG evolving to gastric cancer is of great importance in clinical practice.Aims: To investigate the effect of teprenone,a mucosa protective agent,on expressions of tumor suppressor gene p16 and transforming growth factor-β1(TGF-β1) in the formation and progression of CAG.Methods: Healthy male Wistar rats were randomly assigned into normal control group(n = 20),CAG model group(n = 25) and teprenone intervention group(n = 25).Rats in the latter two groups were administered intragastrically with Helicobacter pylori suspension and alcohol-sodium salicylate solution sequentially to construct CAG model.Rats in teprenone intervention group were given in addition teprenone 50 mg.kg-1.d-1 for 26 weeks.Gross pathological and histopathological changes in gastric mucosa were observed,and the expressions of p16 and TGF-β1 in gastric mucosa were determined by immunohistochemistry.Results: The positive expression rates of p16 protein in normal control group and teprenone intervention group were 95.0% and 73.9%,respectively,both were significantly higher than that in CAG model group(36.4%,P 0.05);while the positive expression rates of TGF-β1 protein in normal control group and teprenone intervention group were 10.0% and 30.4%,respectively,both were significantly lower than that in CAG model group(81.8%,P 0.01).There were no significant differences in p16 and TGF-β1 protein expressions between normal control group and teprenone intervention group.The gastric mucosa was thickened and the number of gastric glands was increased without bleeding and erosion in teprenone intervention group as compared with that in CAG model group.Conclusions: Teprenone can repair the gastric mucosal injury,partially reverse the mucosal atrophy and interrupt the formation and progression of CAG.The mechanism might be partially related to the restoration of expression and function of p16 and down-regulation of TGF-β1 expression.