低氧诱导因子1α在肝癌细胞不同缺氧时间的表达情况及其与血管生成和细胞凋亡的关系  

EXPRESSION OF HIF-1α IN HEPG2 UNDER DIFFERENT HYPOXIA TIME AND ITS RELATIONS WITH VASCULARIZATION AND APOPTOSIS

作　　者：傅志超[1] 程惠华[1] 王凤玫[2] 

机构地区：[1]福州总医院放疗科 [2]上海第二军医大学组织胚胎学教研室

出　　处：《福州总医院学报》2006年第2期90-92,共3页Journal of Fuzhou General Hospital

摘　　要：目的:为了探讨低氧诱导因子-1α(Hypoxia inducible factor-1α,HIF-1α)在不同缺氧时间的肝癌细胞中的表达情况及其与血管生成和细胞凋亡的关系。方法:用氯化钴处理HepG2肝癌细胞模拟缺氧环境,用RT-PCR技术检测缺氧0,1,2,4,6,8h肝癌细胞中的HIF-1α,VEGF,bcl-2的表达,用westernblot方法检测caspase-3蛋白的表达情况。结果:细胞在氯化钴处理后4小时,HIF-1α,VEGF,bcl-2 mRNA达到高峰,随后下降;caspase-3蛋白的表达与前三者正好相反。结论:HIF-1α通过促进VEGF,bcl-2的表达,抑制caspase-3的表达,从而抑制肝癌细胞凋亡,且与缺氧程度有关。HIF-1α在肝癌的发生发展中发挥重要作用。Objective： In order to study the expression of HIF-1α in HepG2 under different hypoxia time and its relations with vascularization and apoptosis. Method： Hypoxia injury was prepared in HepG2 cells which were managed with cobalt chloride, AT 0, 1, 2, 4, 6, 8hours after hypoxia, we measured the expression of HIF- 1α mRNA, VEGF mRNA, bcl - 2 mRNA by RT -PCR, and the expression of Caspase-3 protein. Results： The expression of HIF-1α mRNA, VEGF mRNA, bcl-2 mRNA were increased gradually, peaked at 4h, and then decreased. But the expression of caspase - 3 protein was contrast to the prior three genes. Conclusion： HIF- 1α increased the expression of VEGF and bcl - 2, and decreased the expression of caspase - 3, which inhibited the hepatoma carcinoma cells apoptosis and related to the degree of hypoxia, it play an important role in the caicinogenesis and development of hepotoma.

关 键 词：低氧诱导因子 血管内皮细胞生长因子 bcl-2 CASPASE-3 肝癌 

分 类 号：R373.21[医药卫生—病原生物学]