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目的观察蛋白酶体抑制剂MG132对人肝癌细胞系HepG2的致凋亡作用及其对凋亡相关基因p53蛋白表达的影响。方法采用多个浓度(2,5,10μmol/L)的蛋白酶体抑制剂MG132处理HepG2细胞;流式细胞术和Hoechst荧光染色检测细胞凋亡;免疫细胞化学检测HepG2细胞p53蛋白含量。结果对照组HepG2细胞凋亡率低于5%,在2,5,10μmol/LMG132作用下,细胞凋亡率分别为42.9%,66.1%和72.8%,MG132诱导HepG2细胞凋亡具有剂量—效应关系。经Hoechst荧光染色可见细胞染色质浓缩等凋亡改变。免疫组织化学检测HepG2细胞p53蛋白表达水平增高。结论蛋白酶体抑制剂MG132能够诱导HepG2细胞凋亡,其作用呈剂量—效应关系;p53蛋白表达增加与MG132抑制泛素—蛋白酶体系统降解细胞内p53蛋白有关。
Objective To investigate the effect of proteasome inhibitor MG132 on human hepatocellular carcinoma cell line HepG2 and its effect on the expression of p53 protein. Methods HepG2 cells were treated with multiple concentrations (2,5 and 10 μmol / L) of proteasome inhibitor MG132. Flow cytometry and Hoechst staining were used to detect the apoptosis of HepG2 cells. P53 protein levels in HepG2 cells were detected by immunocytochemistry. Results The apoptotic rates of HepG2 cells in the control group were less than 5%. The apoptotic rates of HepG2 cells were 42.9%, 66.1% and 72.8%, respectively. The apoptosis rates of HepG2 cells treated with 2,5,10μmol / L of LMW132 were dose-dependent . Hoechst staining shows that the chromatin condensation and other apoptosis changes. Immunohistochemical detection of p53 protein expression in HepG2 cells increased. Conclusion The proteasome inhibitor MG132 can induce apoptosis in HepG2 cells in a dose-dependent manner. The increased expression of p53 protein is related to the inhibition of p53 protein degradation by ubiquitin-proteasome system in MG132 cells.