MG132诱导人血管内皮细胞凋亡及对p53表达的影响

Mechanism Involved in the Apoptosis of Human Umbilical Vein Endothelial Cells Induced by Proteasome Inhibitor MG132

目的观察蛋白酶体抑制剂MG132对人血管脐静脉内皮细胞(ECV-304)细胞的致凋亡作用及其对凋亡相关基因p53表达的影响。方法采用两个浓度(2μmol/L,5μmol/L)的蛋白酶体抑制剂MG132处理ECV-304细胞24 h;DNA琼脂糖凝胶电泳检测细胞凋亡,流式细胞术检测细胞凋亡率;免疫细胞化学检测p53蛋白表达。结果对照组ECV-304细胞凋亡率低于5%,在2μmol/L MG132作用下,凋亡率为11.3%±1.2%,MG132浓度升至5μmol/L时,细胞凋亡率增至44.5%±5.3%;免疫组化检测p53蛋白表达水平升高。结论蛋白酶体抑制剂MG132能够诱导血管内皮细胞凋亡,其机制可能与MG132上调p53基因表达有关。

Objective To study the effect of proteasome inhibitor MG132 on expression of p53 in the apoptosis of cultured human umbilical vein endothelial cells induced. Methods Human umbilical vein endothelial cells were treated with MG132 （2 μmol/L, 5 μmol/L） for 24 hours. The apoptotic cells were determined by DNA fragment analysis and flow cytometric analysis, p53 protein expression was detected by immunohistechemistry. Results The results showed that the increase of the degree of human umbilical vein endothelial cells apoptosis was concentration dependent. MG132 could up - regulate the protein expression of p53. Conclusions The results implicated that proteasome inhibitor MG132 induced human umbilical vein endothelial cells apoptosis by inhibitting UPP and accumulation of p53.