论文部分内容阅读
目的:探讨bcl-2表达与端粒酶活性二者之间的调控关系,了解Hp的致癌机制。方法:在Hp培养滤液诱导前后,采用流式细胞仪检测抑制hTERT基因之后SGC7901胃癌细胞bcl-2蛋白的表达。结果:对照组SGC7901胃癌细胞24 h、36 h和48 h表达bcl-2蛋白的阳性细胞率和荧光指数显著低于经Hp培养滤液诱导的SGC7901胃癌细胞组(P<0.05)。在Hp滤液诱导下,抑制hTERT基因的SGC791胃癌细胞24 h、36 h和48 h表达bcl-2蛋白的阳性细胞率和荧光指数与SGC7901胃癌细胞无显著差异(P>0.05)。结论:Hp感染可以促进bcl-2蛋白表达,这可能是Hp感染致胃癌的重要机制之一。端粒酶活化不参与调控bcl-2蛋白表达。
Objective: To investigate the relationship between the expression of bcl-2 and telomerase activity, and to understand the mechanism of Hp carcinogenesis. Methods: The expression of bcl-2 protein in gastric cancer cell line SGC7901 after inhibition of hTERT gene was detected by flow cytometry before and after Hp culture filtrate induction. Results: The positive rate and fluorescence index of bcl-2 protein in SGC7901 gastric cancer cells at 24 h, 36 h and 48 h were significantly lower than those of SGC7901 gastric cancer cells induced by Hp culture filtrate (P <0.05). The SGC7901 gastric cancer cell line SGC791 gastric cancer cells inhibited by hp filtrate induced the expression of bcl-2 protein in 24 h, 36 h, and 48 h after transfection. The positive rate and the fluorescence index of SGC7901 gastric cancer cells were not significantly different (P> 0.05). Conclusion: Hp infection can promote bcl-2 protein expression, which may be one of the important mechanisms of Hp-induced gastric cancer. Telomerase activation is not involved in the regulation of bcl-2 protein expression.