异丙酚对H_2O_2刺激下细胞内ASK1蛋白激活的影响

目的探讨在H2O2刺激下,异丙酚对细胞中Daxx-ASK1信号通路的影响。方法对体外培养的HEK293细胞分为对照组、H2O2刺激组以及H2O2刺激合并异丙酚处理组。采用免疫荧光、Westernblot及MTT等方法,观察异丙酚预处理对H2O2刺激下的HEK293细胞存活率以及细胞中Fas死亡结构域相关蛋白（Daxx）的亚细胞定位以及凋亡信号调节激酶1（ASK1）激活的影响。结果在200～500μmol/LH2O2刺激下,异丙酚在一定程度上能有效保护细胞,缓解抗氧化应激损伤。进一步实验发现,H2O2刺激细胞后,与H2O2刺激组相比,异丙酚处理组细胞中Daxx蛋白大部分仍然聚集在细胞核中,只有少部分移入到细胞浆中,相应ASK1的激活程度也较低。结论氧化应激刺激下,异丙酚可通过抑制细胞中Daxx蛋白的出核,进而抑制胞浆中ASK1蛋白的激活,从而起到保护细胞、抑制细胞死亡的效能。

Effects of propofol on the activation of ASK1 in HEK293 cells

Objective To study the effect of propofol on Daxx-ASK1 signal transduction pathwy in HEK293 cells treated with H2O2.Methods HEK293 cells were devided into three groups：control group,H2O2 treatment group,and H2O2 plus propofol group.Immunofluorescence,Western blot and MTT assays were used to evaluate the cellular viability,subcellular location of Fas death domain-associated protein（Daxx）,and the activation of apoptosis signal-regulating kinase 1（ASK1） in H2O2-treated HEK293 cells.Results At the concentration range of 200-500 mol/L,H2O2 propofol effectively protected cells from H2O2-induced oxidative stress.Furthermore,Daxx was mainly remained in the cytoplasm,and the degree of ASK1 activation was less than the H2O2 treatment group.Conclusion Propofol could protect cells from oxidative stress-induced injury through the inhibition of the translocaton of Daxx and the activation of ASK1.