c-Jun氨基末端激酶活化在三丁基锡诱导凋亡中的作用及机制  

The effect of JNK activation on TBT-induced apoptosis and its possible mechanism

作　　者：张亚莉[1] 孙利军[2] 

机构地区：[1]南通大学医学院生物化学与分子生物学教研室,江苏226001 [2]南通大学公共卫生学院,江苏226001

出　　处：《交通医学》2014年第4期327-330,共4页Medical Journal of Communications

基　　金：江苏省自然科学青年基金(BK20130397;BK20130389);南通大学博士引进人才启动基金(13R26)

摘　　要：目的:研究c-jun氨基末端激酶(JNK)参与三丁基锡(Tributyltin,TBT)诱导正常人羊膜细胞FL凋亡的分子机制。方法:FL细胞经不同浓度TBT染毒1h后,PI/Annexin V双染色法检测FL细胞凋亡率。Western blot检测FL细胞JNK的磷酸化水平,Bax定位、Bcl-2的磷酸化水平及总Bax和Bcl-2表达水平。结果:与对照组相比,4μmol/L和6μmol/L的TBT染毒剂量组细胞凋亡率明显升高,2μmol/L^6μmol/L剂量组JNK磷酸化水平升高,差异有统计学意义(P<0.01)。JNK特异抑制剂SP600125明显降低TBT诱导的FL细胞凋亡率,而JNK特异抑制剂SP600125对Bax定位、Bcl-2的磷酸化水平及总的Bax和Bcl-2表达量无影响。结论:JNK的活化是TBT诱导FL细胞凋亡的重要因素,但JNK介导凋亡的途径并非通过调控凋亡相关因子Bax和Bcl-2。Objective：To study the effects of JNK activation on TBT-induced apoptosis and investigate the underly-ing mechanism in human amnionic cells. Methods：In the study, PI/Annexin V staining assay was applied to detect apopto-sis induced by TBT in FL cells. The phosphorylation of JNK, expression and localization of Bax, and the expression and phosphorylation of the Bcl-2, respectively, were measured by Western blot. Results：Compared with the control group, the proportion of apoptotic FL cells were increased in the 4 and 6 μmol/L TBT-treated groups, and the phosphorylation of JNK was markedly increased in the 2, 3, 4 and 6 μmol/L TBT-treated groups （P〈0.01）. JNK-specific inhibitor attenuated the TBT-mediated elevation of apoptotic rates. However, JNK-specific inhibitor had no effect on the expression and localiza-tion of Bax, as well as the expression and phosphorylation of the Bcl-2. Conclusion：JNK activation in apoptotic human amnion cells is not involved in the upstream signaling of the Bax/Bcl-2-evoked mitochondrial apoptosis pathway.

关 键 词：三丁基锡 凋亡 C-JUN氨基末端激酶 Bax Bcl-2 流式细胞技术 WESTERN BLOT检测 

分 类 号：Q555.7[生物学—生物化学]