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目的探讨中药萎胃康治疗慢性萎缩性胃炎的机制。方法将84只SD大鼠随机分为正常组和造模组。造模组采用水杨酸钠灌胃为主等复合造模法复制大鼠模型。确定造模成功后,造模组大鼠被随机分为模型组,萎胃康大、中、小剂量组和西药组。萎胃康大、中、小剂量组和西药组大鼠分别按照3,1.5,0.75,0.3 g·kg-1的剂量给予相应药物灌胃(ig),每天1次,连续用药30天;正常组和模型组大鼠给予等体积生理盐水。观察各组大鼠胃黏膜组织形态的变化,免疫组化法检测核转细胞周期蛋白E(Cyclin E)和Bcl-2的表达。结果与正常组相比,模型组大鼠Cyclin E和Bcl-2的表达明显增加,具有统计学意义(P<0.05)。与模型组相比,各治疗组大鼠Cyclin E和Bcl-2表达明显减少,差异有统计学意义(P<0.05);与萎胃康小剂量组相比,萎胃康大剂量组大鼠Cyclin E和Bcl-2表达明显减少,差异有统计学意义(P<0.05)。结论中药萎胃康具有治疗慢性萎缩性胃炎的作用,其机制可能与减少Cyclin E和Bcl-2蛋白表达,从而抑制胃黏膜的异常增殖,并防止癌变有关。
Objective To investigate the mechanism of traditional Chinese medicine Weiweikang in treating chronic atrophic gastritis. Methods 84 SD rats were randomly divided into normal group and model group. Model group using sodium salicylic acid-based compound modeling rat model. After confirming the success of modeling, the model rats were randomly divided into model group, Weiweikang large, medium and small dose group and western medicine group. Weweikang large, medium and small dose group and Western medicine group rats were given the corresponding drug 3,1.5,0.75,0.3 g · kg-1 dose (ig), once daily for 30 days; normal Group and model rats were given equal volume of saline. The morphological changes of gastric mucosa in each group were observed. The expressions of Cyclin E and Bcl-2 were detected by immunohistochemistry. Results Compared with normal group, the expressions of Cyclin E and Bcl-2 in model group were significantly increased (P <0.05). Compared with the model group, the expression of Cyclin E and Bcl-2 in each treatment group decreased significantly, the difference was statistically significant (P <0.05); Compared with the low dose Weiweikang group, the rats in the high dose Weiweikang group Cyclin E and Bcl-2 expression was significantly decreased, the difference was statistically significant (P <0.05). Conclusion Chinese medicine Weiweikang can treat chronic atrophic gastritis. Its mechanism may be related to reducing the expression of Cyclin E and Bcl-2 protein, inhibiting the abnormal proliferation of gastric mucosa and preventing the carcinogenesis.