丙泊酚对高糖环境下心肌细胞缺氧后损伤的保护作用

摘要

Objective To study the protective effect of propofol on post-hypoxic injury of car-diomyocytes induced during hyperglycemia.Methods Rat primary H9C2 cardiomyocytes were cul-tured and the model of hypoxia-reoxygenation (HR)was constructed.The cells were assigned to the following groups:normal control group (group NC),high glucose group (group HG)and HR under high glucose group (group GR),and propofol treated groups in which cells were treated with various concentrations (12.5,25,50,and 100 μmol/L)of propofol (i.e.,groups P12.5,P25,P50 and P100)and the solvent DMSO group (D100 group,DMSO at 100 μmol/L)respectively.(CK-MB), cardiac troponin I (cTnI),lactate dehydrogenase (LDH),mitochondrial activity,intracellular ATP content and intracellular oxidation of the cells were compared.Results Compared with the groups NC and HG,the cell viability was significantly decreased,the concentration of LDH and MDA,relative concentration of CK-MB and cTnI increased significantly,and the activity of T-SOD,mitochondria and the relative concentration of ATP decreased significantly in the other groups (P<0.05).Com-pared with the group GR,the cell activity increased significantly,the concentration of LDH and MDA ,relative concentration of CK-MB and cTnI were Significantly decreased,and the activity T-SOD, mitochondrial and relative concentration of ATP increased significantly in the groups P12.5,P25 and P50 (P<0.05).Compared with the group P25,the cell viability decreased significantly,the concen-trations of LDH,MDA,relative concentrations of CK-MB and cTnI increased significantly,and the activity of T-SOD and mitochondria and relative concentration of ATP were significantly reduced in the groups P50,P100 and D100 (P<0.05).Conclusion Propofol can reduce the damage of myocar-dial cells by reducing the damage of mitochondria.%目的 研究丙泊酚对高糖环境下心肌细胞缺氧后损伤的保护作用.方法 培养大鼠原代 H9C2 心肌细胞,构建细胞缺氧-复氧模型.将这些心肌行实验分组:正常培养组(NC 组)、高糖培养组(HG组)、高糖缺氧-复氧组(GR组),在高糖缺氧-复氧环境下,培养基中分别加入终浓度分别为 12.5 μmol/L(P12.5 组)、25 μmol/L(P25 组)、50 μmol/L(P50 组)以及 100 μmol/L(P100 组)的丙泊酚以及终浓度为 100 μmol/L的二甲基亚砜(DMSO)溶剂组(D100 组).检测各组的细胞活力、肌酸激酶-MB(CK-MB)、心肌肌钙蛋白I(cTnI)、乳酸脱氢酶(LDH)浓度以及细胞内氧化应激水平和线粒体依赖性细胞凋亡水平.结果 与 NC 和 HG 组比较,其余组的细胞活力明显降低,LDH、MDA浓度、CK-MB和 cTnI 相对浓度明显升高,T-SOD、线粒体活性和 ATP 相对浓度明显降低(P<0.05);与 GR组比较,P12.5 组、P25 组、P50 组细胞活力明显升高,LDH、MDA 浓度、CK-MB和 cTnI相对浓度明显降低,T-SOD、线粒体活性和 ATP 相对浓度明显升高(P<0.05);与 P25 组比较,P50 组、P100 组以及D100 组细胞活力明显降低,LDH、MDA 浓度、CK-MB 和 cTnI 相对浓度明显升高,T-SOD、线粒体活性和 ATP相对浓度明显降低(P<0.05).结论 一定浓度的丙泊酚可以通过减轻氧化应激,减少线粒体的损伤从而减轻高糖缺氧对心肌细胞的损伤.