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[目的] 探讨盐酸小檗碱对实验性大鼠胃癌前病变的影响及与细胞凋亡和P53、Bcl -2 蛋白、mRNA表达水平的关系。[方法] 采用N -甲基- N -亚硝基胍饮水法建立大鼠胃癌前病变模型,用盐酸小檗碱预防和大、中、小3种剂量干预治疗,观察大鼠的一般情况,以光镜观察胃癌前病变的发生率,并运用末端DNA标记法检测凋亡率(AI),免疫组化法检测细胞中P53 和Bcl -2 蛋白表达,逆转录多聚酶链式反应检测P53 和Bcl- 2 的mRNA水平。[结果] 经盐酸小檗碱干预大鼠,其癌前病变的发生率明显降低,与模型组比较P<0.05,AI显著提高,3 种剂量组与模型组比较均P<0.05,并伴有Bcl- 2、突变型P53基因蛋白表达水平降低,野生型P53 基因mRNA水平升高,Bcl -2基因mRNA水平下调,其中以大剂量组尤为显著,与模型组比较P<0.01。[结论] 盐酸小檗碱能预防和治疗实验性大鼠胃癌前病变,其机制与提高细胞凋亡率和调控基因表达有关。
[Objective] To investigate the effect of berberine hydrochloride on gastric precancerous lesions and its relationship with apoptosis, P53, Bcl-2 protein and mRNA expression in gastric cancer in rats. [Methods] The model of gastric precancerous lesions in rats was established by N - methyl - N - nitrosoguanidine drinking water. Berberine hydrochloride was used to prevent and treat the gastric cancer in rats. The general condition, The incidence of gastric precancerous lesions was observed with light microscope, and the apoptosis rate (AI) was detected by terminal DNA labeling. The expression of P53 and Bcl-2 protein was detected by immunohistochemistry. The expressions of P53 and Bcl- - 2 mRNA levels. [Result] The incidence of precancerous lesion in berberine hydrochloride group was significantly lower than that in model group (P <0.05, AI), and the three dose groups were significantly lower than those in model group (P <0.05) The expression of Bcl-2, mutant P53 protein decreased, the level of wild-type P53 mRNA increased, and the level of Bcl-2 mRNA decreased, especially in the high dose group, P <0.01 compared with the model group. [Conclusion] Berberine can prevent and treat gastric precancerous lesions in experimental rats, and its mechanism is related to the increase of apoptosis rate and regulation of gene expression.