镉诱导大鼠肾细胞凋亡及其机理的研究  

Study on the Mechanisms of NRK Cells Apoptosis Induced by Cadmium

作　　者：贾广乐[1] 王众[1] 吴绍强[1] 林祥梅[1] 韩雪清[1] 刘建[1] 梅琳[1] 张旻[1] 

机构地区：[1]中国检验检疫科学研究院,北京100029

出　　处：《生态毒理学报》2008年第3期268-273,共6页Asian Journal of Ecotoxicology

基　　金：国家科研院所基本科研业务费资助项目(No. 2007JK022)

摘　　要：为探讨镉(Cd)致大鼠肾细胞(NRK cell)凋亡的死亡受体途径,分别将终浓度为0、10、20、40、60μmol·L-1的CdCl2添加到培养液中,对NRK细胞暴露6h.应用流式细胞仪检测NRK细胞凋亡率;分光光度计检测Caspase-8蛋白活性;半定量RT-PCR检测Caspase-8、Fas的mRNA表达.结果表明,随着CdCl2暴露浓度的升高,NRK细胞凋亡率升高,Caspase-8蛋白活性增强,Caspase-8、Fas的mRNA表达增强,并呈现剂量-效应关系.说明镉可以通过死亡受体这条通路来引起NRK细胞凋亡.In order to study the death-receptor pathway in NRK cell apoptosis induced by cadmium, different concentrations of cadmium chloride （0, 10, 20, 40, 60 μmol·L^-1） were added to NRK cell culture medium and cultured for 6h. Apoptosis rate, Caspase-8 activity and expression level of mRNA of Caspase-8 and Fas were detected by flow cytometry, spectrophotometer and RT-PCR, respectively. Results showed that concomitant dose-dependent increases in apoptosis rate, Caspase-8 activity and the expression level of Caspase-8 and Fas mRNA were found, which indicated apoptosis of NRK cells could be induced by cadmium through death-receptor pathway.

关 键 词：镉 NRK细胞 死亡受体途径 

分 类 号：Q813[生物学—生物工程]