P38MAPKc、aspase-8在Fas-放线菌素D诱导Bel-7402细胞凋亡中的作用

The roles of P38MAPK and caspase-8 in Fas-and actinomycin D-induced apoptosis of Bel-7402 cells

目的确定P38MAPKc、aspase-8的关系,以探讨Fas-actinomycin D(Fas-AD)诱导Bel-7402细胞凋亡的信号转导机制。方法通过流式细胞仪检测Fas-AD、SB203580(P38MAPK特异性抑制剂)及Ac-IEFD-cho(caspase-8特异性抑制剂)对Bel-7402细胞凋亡的影响;通过Western-blot法检测Fas-AD、SB203580及Ac-IEFD-cho对培养的Bel-7402细胞的P38MAPK、caspase-8的激活及其表达的影响。结果Fas-AD能明显诱导Bel-7402细胞凋亡,SB203580和Ac-IEFD-cho能明显抑制Fas-AD诱导的细胞凋亡。Fas-AD能诱导P38MAPK、caspase-8激活并表达,而SB203580和Ac-IEFD-cho能分别抑制它们的激活及表达。结论在Bel-7402细胞凋亡中,P38MAPK与caspase-8参与Fas-AD凋亡途径,并且相互调节。

Objective To ensure the relationship between P38MAPK and caspase-8, and to discuss the signal transducfion mechanism of the Bel-7402 cells＇ apoptosis induced by Fas-actinomycin D（Fas-AD）, through the interaction between SB203580 and Ac-IEFD-cho.Methods Bel-7402 cells were treated with Fas-AD for 24 h in the presence/absenee of caspase-8 inhibitor Ae-IEFD-cho or SB203580. Cell apoptosis was evaluated by flow eytometry （FCM） and the expressions of P38MAPK and caspase-8 were determined by Western blot, respectively.Results Compared with the controlgroup, after being treated with Fas-AD,the apoptosis rate of Bel-7402 ,cell and the expressions of activated caspase-8 and P38MAPK increased significantly. However, after being treated with Fas-AD in the.prsence of the caspase-8 inhibitor Ac-IEFD-cho or P38MAPK inhibitor SB203580, the apoptosis rate of Bel-7402 cell and the expressions of activated caspase-8 and P38MAPK decreased. Conclusion P38MAPK and caspase-8 are involved in Fas-AD apoptotic pathway and interact after Bel-7402 cells are treated with Fas-AD.