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目的:探讨胃炎Ⅰ号方对慢性萎缩性胃炎(CAG)的疗效及其分子机制。方法:90只SD大鼠随机分为正常对照组、模型组、胃炎Ⅰ号(1.08,0.54 g.kg-1)治疗组;除正常对照组外,所有大鼠进行CAG造模,20周后开始ig给药,1次/d,连续12周后处死大鼠,胃黏膜组织切片观察病变程度,采用RT-PCR测定β-链蛋白(β-catenin)和周期素D1(cyclin D1)表达水平。结果:模型组大鼠胃黏膜出现CAG病变,治疗组大鼠CAG病变减轻;CAG大鼠模型组β-catenin和cyclin D1表达较正常对照组升高(P<0.01),治疗组β-catenin和cyclin D1表达明显低于模型组(P<0.01)。结论:胃炎I号对CAG有治疗作用,β-catenin和cyclin D1在CAG模型中表达升高,胃炎Ⅰ号方可能通过抑制β-catenin和cyclin D1治疗CAG。
Objective: To investigate the curative effect and molecular mechanism of gastritis I on chronic atrophic gastritis (CAG). Methods: Ninety SD rats were randomly divided into normal control group, model group and gastritis Ⅰ (1.08,0.54 g.kg-1) treatment group. All rats except the normal control group were subjected to CAG modeling. After 20 weeks The rats were sacrificed after 12 weeks of continuous ig administration once a day for 12 weeks. The pathological changes of gastric mucosa were observed. The expression of β-catenin and cyclin D1 were determined by RT-PCR. . Results: The CAG lesion was found in gastric mucosa in model group and the CAG lesion in treatment group was alleviated. The expression of β-catenin and cyclin D1 in CAG model group was higher than that in normal control group (P <0.01) cyclin D1 expression was significantly lower than the model group (P <0.01). Conclusion: Gastritis I can treat CAG. Β-catenin and cyclin D1 are up-regulated in CAG model. Gastritis I can inhibit CAG by inhibiting β-catenin and cyclin D1.