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作 者:王国安[1] 刘海峰[2] 房殿春[1] 腾小春[1] 何俊堂 陈刚[1]
机构地区:[1]第三军医大学西南医院全军消化专科中心,重庆400038 [2]武警总医院消化内科,北京100039
出 处:《西南国防医药》2006年第1期14-16,共3页Medical Journal of National Defending Forces in Southwest China
基 金:军队医药卫生"九五"重点课题资助项目NO.96Z047;重庆市应用基础研究基金资助项目;NO.1998-06
摘 要: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 explore the relationship between the activity of telomerase and the expression of bcl - 2 protein and to study the carcinogenic mechanism of H. pylori. Methods: The expression of bcl - 2 protein in SGC7901 cells transferred antisense hTERT was detected by flow eytometryanalysator(FCM) in the presence of low concentration of H. pylori incubating filtrate. Results: The rate of cells and the fluorescent index of expressing bcl - 2 protein in the control SGC7901 cells were significantly lower than those in SGC7901 cells culture with H. pylori filtrate in 24 , 36 and 48 h(P〈0. 05). It was not remarkable the differences of the rate of cells and fluorescent index of expressing bcl - 2 protein between SGC7901 cells and SGC7901 cells transferred anrisense hTERT both cultured with H, pylori filtrate in 24, 36 and 48 h(P〉0.05). Conclusion: H. pylori infection could promote the expression of bcl - 2 protein in the SGC7901 cell, which may he an important cancerigenic mechanism of H. pylori. Telomerase does not take part in the regulation of the expression of bcl - 2 protein.
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