H_2O_2致Hep-G2细胞凋亡及其分子机制初探  

Molecular events associated with cell apoptosis and Tissue damage induced by H_2O_2 in Hep-G2

作　　者：冯莉[1] 苏奉发[1] 李丽[1] 任碧轩[1] 杨健[1] 张大容[1] 唐恩洁[1] 

机构地区：[1]川北医学院免疫与分子生物研究所,四川南充637000

出　　处：《川北医学院学报》2005年第1期6-10,共5页Journal of North Sichuan Medical College

摘　　要：目的本研究旨在探索H2O2 诱导Hep-G2发生凋亡及其致凋亡发生的分子机制。方法采用免疫细胞化学技术与特异性抗体初步探索了经H2O2 处理的Hep-G2细胞Fas、bcl-2、P53、P21、Caspase3等与细胞凋亡和生长抑制基因的表达情况。结果检测结果表明H2O2 处理的Hep-G2细胞的Fas和Caspase3基因表达增加, bcl-2基因表达减少,而P53、P21基因的表达未见明显改变,提示Fas、Caspase3和bcl-2基因在H2O2 诱导的细胞凋亡中起重要作用;bcl-2通过抑制诱导凋亡所致的细胞永生化,可能在肿瘤的发生、发展中起重要作用。P53、P21、保持不变,可能反映了H2O2 诱导的细胞凋亡不依赖P53途径。Objective H 2O 2 is the oxidant to induce DNA damage and cell apoptosis. In order to investigated the Molecular events associated with cell apoptosis and tissue damage induced by H 2O 2。Methods We used Immunocytochemistry technique and specific antibodies to measure the expression of p53、 p21、 bcl-2、Fas and caspase3 in Hep-G2 after treating with H 2O 2 . Results The results indicated the expression of Fas、caspase 3 were increased,but The expression of bcl-2 was reduced at 1h,3h,6h,8h,24h,36h after treatment, P53 and P21 was kept to unchanged. Moreover, an increase in the apoptotic activity was caused. These results suggest that Up-regulation of Fas and caspase 3 and down- regulation were involved in the altered balance between survival and apoptosis induced by H 2O 2.

关 键 词：细胞凋亡 分子机制 CASPASE3 Hep-G2细胞 bcl-2基因 H2O2诱导 免疫细胞化学技术 生长抑制基因 特异性抗体 P21基因 细胞永生化 P53途径 Fas 初步探索 表达情况 基因表达 检测结果 表达减少 诱导凋亡 

分 类 号：R735.7[医药卫生—肿瘤] R363[医药卫生—临床医学]