镉致293细胞凋亡过程中JNK信号传导通路与Bax基因关系研究  

Study on the Relationship of JNK Signaling Pathway and Bax on 293 cell apoptosis induced by cadmium

作　　者：喻道军[1] 徐兆发[2] 

机构地区：[1]沈阳医学院公共卫生学院,辽宁沈阳110034 [2]中国医科大学公共卫生学院

出　　处：《现代预防医学》2012年第8期1976-1977,共2页Modern Preventive Medicine

基　　金：国家自然科学基金资助项目(30371200)

摘　　要：目的利用RNAi技术探讨JNK、c-Jun、Bax基因在镉致293细胞凋亡过程中的作用及相互关系。方法细胞转染siRNA-JNK或siRNA-Bax后染镉,用Western blotting法测基因蛋白表达,流式细胞术测细胞凋亡。结果 30μmol/L氯化镉可使293细胞相关基因表达明显增高,细胞凋亡增加。siRNA-JNK可抑制这些效应,而siRNA-Bax只能抑制Bax表达和细胞凋亡,对其他基因无明显影响。结论 JNK信号传导通路可能通过上调Bax基因表达促进细胞凋亡。OBJECTIVE To study the effects of JNK,c-Jun,Bax genes and the relationship among them on 293 cell apoptosis induced by cadmium chloride with RNAi.METHODS Cells were incubated with CdCl2 after siRNA-JNK and siRNA-Bax transfection.The protein expressions of genes were detected by western blot,and the rate of apoptosis was measured by flow cytometry.RESULTS The apoptosis rate of 293 cell treated with 30μmol/L CdCl2 was higher than those of the control accompanied by increased expressions of genes.Silence of JNK could inhibit those changes,while siRNA-Bax could only inhibit the expression of Bax and apoptosis,and had no significant effect on other gene.CONCLUSION The results suggested that JNK Signaling Pathway mediated 293 cells apoptosis induced by cadmium chloride via improving the expression of Bax gene.

关 键 词：镉 JNK Bax 基因沉默 

分 类 号：R34[医药卫生—基础医学]