目的：研究丙泊酚对 H2 O2诱发的心肌细胞损伤的保护作用及其作用机制。方法采用胰酶消化法获取大鼠胎鼠心肌细胞，以 H2 O2损伤心肌细胞获得心肌缺血再灌注损伤实验模型；加入不同浓度丙泊酚（12.5、25、50μmol·L -1），MTT 法检测细胞存活率；用硫代巴比妥酸法、黄嘌呤氧化酶法分别测定各组细胞培养液中丙二醛（MDA）含量及超氧化物歧化酶（SOD）活性；流式细胞术检测细胞凋亡水平；Western blotting 检测细胞中 ERK1/2、Bcl -2及 Bax 的表达。结果丙泊酚（12.5、25、50μmol·L -1）能抑制由 H2 O2导致的细胞死亡（P <0.01）；减少MDA 的产生（P <0.01），提高 SOD 活性（P <0.01）；25、50μmol·L -1丙泊酚能抑制由 H2 O2导致的细胞凋亡（P <0.05）；25μmol·L -1丙泊酚作用于细胞后能激活 ERK1/2磷酸化，增加 Bcl -2且减少 Bax 的表达。结论丙泊酚通过激活 ERK1/2磷酸化对 H2 O2诱发的心肌细胞损伤起到保护作用。%Objective To investigate the influence and mechanism of propofol on cardiomyocytes damaged by H2 O2 . Methods Cardiomyocytes from the hearts of 1 ~ 3 - day - old neonatal rats were prepared by a modified method. Treated cultured rat cardiomyocytes by H2 O2 ,propofol(12. 5,25,50 μmol·L - 1 ). MTT was used to detect cell viability. Malondial-dehyde(MDA)was determined by measuring thiobarbituric acid - reactive substances. Superoxide dismutase(SOD)was assayed by xanthine oxidase method. The rates of apoptosis of cardiomyocyte were detected by flow cytometry. The expression of ERK1 / 2,Bcl - 2 and Bax were tested by western blotting. Results Propofol suppressed the cardiomyocyte death induce by H2 O2(P < 0. 01),and decreased the production of MDA(P < 0. 01),promoted the ability of SOD(P < 0. 01). The ap-optosis rates of propofol group significant different from that of H2 O2 group(P < 0. 05). Propofol activated the phosphorated ERK1 / 2. The expression of Bcl - 2 was increased while that of Bax was suppressed. Conclusion Propofol protected on cul-tured rat cardiomyocytes damaged by H2 O2 via ERK1 / 2 signal pathway.
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