丙泊酚抑制H_2O_2诱导的肝L02细胞凋亡

Propofol Inhibited the Apoptosis of Human Hepatic L02Cells Induced by H_2O_2

目的:探讨丙泊酚在H2O2诱导的人肝L02细胞凋亡中的作用。方法:人肝L02细胞经丙泊酚预处理后再用H2O2进行处理,采用TUNEL法及caspase-3切割程度来检测细胞的凋亡。通过real-time PCR检测Bcl-2(B-cell lymphoma 2),BclxL(B-cell lymphoma-extra large),Bad(Bcl-2-associated death promoter)和Bax(Bcl-2-associated X protein)mRNA表达量。结果:在H2O2诱导的凋亡过程中,经丙泊酚预处理的L02细胞凋亡数量及caspase-3切割量均明显减少。并且这种减少与丙泊酚的剂量成正相关:当丙泊酚剂量用至300μmol/L时,细胞的凋亡程度被降至最低。丙泊酚预处理减少了促凋亡基因Bad和Bax的mRNA表达。结论:丙泊酚对H2O2诱导的人肝细胞L02凋亡具有抑制作用,可能部分是通过抑制Bad和Bax的表达发挥作用的。

Objective：To explore the effect of propofol in H2 O2-induced apoptosis of human hepatic L02 cells.Methods：Preconditioned or nonpreconditioned human hepatic L02 cells were exposed to H2 O2 and the apoptosis was evaluated by TUNEL assay and caspase-3 cleavage.The mRNA expressions of Bcl-2,Bcl-xL,Bad,and Bax were quantified by real-time PCR.Results：Propofol preconditioning reduced population of apoptotic cells and caspase-3 cleavage induced by H2O2in L02 cells,which was positively correlated to the dosage of propofol.When a dose of propofol to 300μmol/L,apoptosis of the cells were reduced to a minimum degree.Propofol pretreatment decreased the expressions of pro-apoptotic genes Bad and Bax mRNA.Conclusions：Propofol protect against H2 O2-induced apoptosis in hepatic cells L02,which is partly mediated by suppressing expression of Bad and Bax.