摘要
目的:探讨c-Jun氨基末端激酶(c-Jun N-terminal kinase,JNK)信号传导通路特异阻断剂sp600125对乙醛刺激的大鼠肝星状细胞株(HSC-T6)凋亡以及Fas蛋白表达的影响。方法:不同浓度sp600125对乙醛刺激的大鼠HSC-T6进行处理后,用Hoechst 33258染色后,观察凋亡细胞的形态变化,FCM法检测细胞凋亡率,SABC法检测Fas蛋白表达。结果:不同浓度的sp600125能诱导乙醛刺激的HSC-T6凋亡,表现为细胞核浓缩、碎裂,形成凋亡小体;随着sp600125浓度增加,HSC-T6凋亡率逐渐增高(F=42.57,P<0.01),HSC-T6细胞内Fas蛋白阳性表达率也逐渐增高(F=72.58,P<0.01)。结论:不同浓度sp600125能诱导乙醛刺激的HSC-T6凋亡,这可能与上调Fas蛋白表达有关。
Objective：To study the effects of sp600125, a special inhibitor of C - Jun terminal kinase（JNK）, on apoptosis and protein expression of Fas stimulated by acetaldehyde in hepatic satellite cells（ HSC）and the roles of JNK in liver fibrosis. Methods： HSC - T6 stimulated by acetaldehyde were exposed to sp600125 at different doses. The shape of HSC- T6 was observed by Hoechst 33258,the rate of HSC - T6 apoptosis was analyzed by FCM, the protein expression of Fas was examined by SAJ3C. Results： sp600125 could induce the apoptosis of HSC - T6. It was showed that the nucleus of HSC - T6 was concentrated and fragmented and the apoptotic body was formed. As the dose of sp600125 increased.the rate of HSC - T6 apoptosis increased gradually（F=42. 57,P〈0. 01） and the protein expression of Fas also increased by degrees（F=72. 58,P〈0. 01 ）. Conclusion：sp600125 could accelerate HSC - T6 apoptosis, which maybe resulted from the up - regulated expression of Fas proteiru
出处
《西南国防医药》
CAS
2008年第3期334-336,共3页
Medical Journal of National Defending Forces in Southwest China
