丙泊酚对H2O2诱导的大鼠心肌细胞程序性坏死的影响  

Effect of propofol on H2O2-induced necroptosis in rat cardiomyocytes

作　　者：阴文超 贾海滨 吴文知[1] 张兰[1] 王春燕 Yin Wenchao;Jia Haibin;Wu Wenzhi;Zhang Lan;Wang Chunyan(Department of Anesthesiology,Sichuan Orthopedic Hospital,Chengdu 610041,China;Department of Anesthesiology,Shenzhen People's Hospital,Shenzhen 518020,China)

机构地区：[1]四川省骨科医院麻醉科,成都610041 [2]深圳市人民医院麻醉科,518020

出　　处：《中华麻醉学杂志》2019年第11期1376-1378,共3页Chinese Journal of Anesthesiology

基　　金：国家自然科学基金(81801947)。

摘　　要：目的评价丙泊酚对H2O2诱导的大鼠心肌细胞程序性坏死的影响。方法取对数生长期的H9C2大鼠心肌细胞,采用随机数字表法将细胞分为4组(n=9):对照组(C组)、H2O2组、丙泊酚组(P组)和二甲基亚砜组(D组)。C组细胞正常培养;H2O2组向细胞培养基中加入H2O2,终浓度为500μmol/L;P组和D组于加入H2O2前30 min,分别向细胞培养基中加入丙泊酚终浓度50μmol/L和等容量的二甲基亚砜。细胞培养或H2O2孵育12 h后,采用碘化丙啶法确定细胞坏死率,采用DCFH-DA染色测定细胞ROS水平,采用Western blot法检测受体相互作用的丝氨酸/苏氨酸蛋白激酶1(RIPK1)、RIPK3、混合谱系激酶结构域样蛋白(MLKL)的表达。结果与C组比较,H2O2组和D组坏死率和ROS水平升高,RIPK1、RIPK3和MLKL表达上调(P<0.05);与H2O2组比较,P组坏死率和ROS水平降低,RIPK1、RIPK3和MLKL表达下调(P<0.05)。结论丙泊酚可减轻H2O2诱导的大鼠心肌细胞程序性坏死。Objective To evaluate the effect of propofol on H2O2-induced necroptosis in rat cardiomyocytes.Methods H9C2 cells at the logarithmic growth phase were divided into 4 groups(n=9 each)using a random number table method:control group(group C),H2O2 group,propofol group(group P)and dimethyl sulfoxide group(group D).Cells were incubated in normal DMEM medium in group C.H2O2 was added to the culture medium with the final concentration of 500μmol/L in group H2O2.Propofol at the final concentration of 50μmol/L and the equal volume of dimethyl sulfoxide were added to the cell medium at 30 min before H2O2 exposure in group P and group D,respectively.After 12-h culture or incubation with H2O2,cardiomyocytes necrosis was detected by PI staining,reactive oxygen species(ROS)level was determined by DCFH-DA staining,and the expression of receptor-interacting serine/threonine-protein kinase 1(RIPK1),RIPK3 and mixed lineage kinase domain-like protein(MLKL)was determined by Western blot.Results Compared with group C,necrosis rate and ROS level were significantly increased,and the expression of RIPK1,RIPK3 and MLKL was up-regulated in H2O2 and D groups(P<0.05).Compared with group H2O2,necrosis rate and ROS level were significantly decreased,and the expression of RIPK1,RIPK3 and MLKL was down-regulated in group P(P<0.05).Conclusion Propofol can attenuate H2O2-induced necroptosis in cardiomyocytes of rats.

关 键 词：二异丙酚 过氧化氢 肌细胞 心脏 坏死 

分 类 号：R614[医药卫生—麻醉学]