摘要
目的 研究融合蛋白IFNγ LTα诱导L92 9细胞凋亡的信号转导机制 ,并与LTα相比较。方法 用结晶紫染色法观察细胞毒效应 ;用检测试剂盒检测caspase 8和 3活性的变化 ;观察 3种信号转导分子的抑制剂对IFNγ LTα和LTα诱导的细胞毒效应的影响。结果 IFNγ LTα能诱导L92 9细胞凋亡及胞内caspase 8和 3的活性变化 ,但两种caspase产生的时间和幅度有所不同。PKC的抑制剂可促进IFNγ LTα和LTα对L92 9细胞的杀伤 ;而PLA2及Ca2 +通道的抑制剂对杀伤则有明显的阻断作用 ,但对LTα的阻断强于对IFNγ LTα的阻断。结论 IFNγ LTα融合蛋白的抗肿瘤活性强于LTα ,其信号转导特征有别于LTα。信号分子caspase与PKC、PLA2、Ca2
Aim To study the signal transduction mechanism in apoptosis of L929 cell induced by IFNγ-LTα and compare it with that induced by LTα. Methods The changes in activities of caspase 8 and caspase 3 in L929 cells were detected. The effects of 3 inhibitors of signal transduction molecule on the cytotoxicity of IFNγ-LTαand LTα were observed. Results The cytotoxic rate of IFNγ-LTα was higher than that of LTα. The activities of caspase 8 and caspase 3 changed upon induction by IFNγ-LTα and LTα. The inhibitor of PKC could promote the L929 cell apoptosis and inhibitors of PLA2 and Ca 2+ channel could block the apoptosis. But the blocking effect was more evident for LTα induced apoptosis than IFNγ-LTα induced apoptosis. Conclusion Anti-tumor activity of the fusion protein IFNγ-LTα is stronger than that of LTα. Signal transduction in apoptosis induced by IFNγ-LTα may be different from that induced by LTα.
出处
《细胞与分子免疫学杂志》
CAS
CSCD
北大核心
2002年第5期435-438,共4页
Chinese Journal of Cellular and Molecular Immunology
基金
浙江省自然科学基金资助
No .3980 80
国家自然科学基金资助课题
No .396 70 875
