在Fas诱导Bel-7402细胞凋亡中p38MAPK调节Bcl-2的表达  

p38 mitogen-activated protein kinase modulates Bcl-2 expression during FAS-induced apoptosis in Be1-7402 cells

作　　者：王玉[1] 孙黎光[1] 夏春辉[2] 叶丽平[1] 张莹[1] 

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,辽宁省沈阳市110001 [2]齐齐哈尔医学院,黑龙江省齐齐哈尔市161042

出　　处：《世界华人消化杂志》2007年第30期3184-3189,共6页World Chinese Journal of Digestology

基　　金：辽宁省教育厅科研基金;No.2004D173;黑龙江省普通高等学校骨干教师创新能力资助计划;No.1054G070~~

摘　　要：目的:探讨p38MPAK是否参与Fas和AD诱导Bel-7402细胞的凋亡过程,以及p38MPAK和bcl-2的关系,进一步揭示p38MAPK的凋亡途径.方法:在Fas和AD作用24h后,用MTT法检测Bel-7402细胞的活力,用Western-blot和RT- PCR法检测p38MAPK,p-p38MAPK和Bcl-2 expression,用免疫荧光法对p-p38MAPK进行细胞定位.结果:随着Fas浓度的增加,Bel-7402细胞的活力明显抑制,p38MAPK和p-p38MAPK表达明显增高(P<0.01),且p-p38MAPK由胞质易位到胞核.Bcl-2的表达明显降低(P<0.01),并且这种降低趋势被p38MAPK抑制剂SB203580所阻止.结论:p38MAPK参与Fas诱导的凋亡途径,以磷酸化形式激活后抑制Bcl一2的表达,进而促进细胞凋亡.AIM： To investigate whether p38 mitogenactivated protein kinase （p38MAPK） is involved in Fasand actinomycin D （AD）-induced apoptosis in Bel-7402 cells, and the relationship between p38MAPK and Bcl-2 expression. METHODS： We measured the viability of Bel-7402 cells by MTT assay, p38MAPK, p-p38MAPK and Bcl-2 expression by Western blotting and reverse transcription polymerase chain reaction （RT-PCR）, and the location ofp-p38MAPK in Bel-7402 cells after Fas and AD treatment by immunofluorescene. RESULTS： Bel-7402 cell viability was significantly inhibited by Fas （P 〈 0.01）. p38MAPK and p-p38MAPK increased significantly with increasing Fas （P 〈 0.01）, leading to cell death as assessed by MTT after 24 hours of Fas and AD treatment, p-p38MAPK translocation into the nucleus was dependent on Fas stimulation. Bcl-2 expression decreased significantly and was prevented by SB203580 during Fas- and ADinduced apoptosis （P 〈 0.01）. CONCLUSION： p38MAPK is involved in Fasand AD-induced apoptosis, and p38MAPK modulates Bcl-2 expression during this apoptosis pathway.

关 键 词：P38MAPK P-P38MAPK Bcl-2 细胞凋亡 免疫印迹 逆转录聚合酶链式反应 FAS 

分 类 号：R363[医药卫生—病理学] R73-3[医药卫生—基础医学]