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

作　　者：王玉[1] 孙黎光[1] 王璐[2] 

机构地区：[1]中国医科大学基础医学院生物化学与分子生物学教研室 [2]哈尔滨医科大学国际遗传学杂志编辑部,黑龙江哈尔滨150081

出　　处：《哈尔滨医科大学学报》2008年第3期216-220,共5页Journal of Harbin Medical University

基　　金：国家自然科学基金(39970651);辽宁省教育厅科研基金(2004D173);黑龙江省自然科学基金(D2007-114)

摘　　要：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.

关 键 词：FAS CASPASE-8 P38MAPK 凋亡 

分 类 号：Q255[生物学—细胞生物学]