异丙酚对大鼠心肌细胞氧化损伤时血红素加氧酶-1表达的影响

目的 探讨异丙酚对大鼠心肌细胞氧化损伤时血红素加氧酶-1(HO-1)表达的影响.方法 培养1周的乳鼠心肌细胞按9×10~4/ml接种在96孔培养板上,每孔0.1 ml,随机分为8组,每组6孔:对照组(C组)、H_2O_2组(H组)、低剂量异丙酚组(LP组)、中剂量异丙酚组(MP组)、高剂量异丙酚组(HP)、低剂量异丙酚+抑制剂组(LP+I组)、中剂量异丙酚+抑制剂组(MP+I组)、高剂量异丙酚+抑制剂组(HP+I组).抑制剂采用ZnPP IX.各组于孵育6 h后,测定心肌细胞丙二醛(MDA)含量、超氧化物歧化酶(SOD)、线粒体、Caspase-3的活性及HO-1 mRNA表达.结果 与C组比较.其余各组心肌细胞MDA含量上升、SOD含量及线粒体活性降低;H组心肌细胞Caspase-3活性升高、HO-1 mR-NA表达上调;不同剂量异丙酚组心肌细胞HO-1 mRNA表达上调;不同剂量异丙酚组经ZnPP Ⅸ处理后心肌细胞Caspase-3活性升高,均P<0.05或P<0.01.与H组比较,不同剂量异丙酚组心肌细胞MDA含量降低、SOD活性升高、线粒体活性升高,MP组和HP组心肌细胞Caspase-3活性降低、细胞HO-1 mRNA表达上调(P<0.05或P<0.01).与相应剂量异丙酚组比较,经ZnPP IX处理后心肌细胞MDA含量升高、SOD活性降低、线粒体活性降低、HO-1 mRNA 表达下调,MP+I、HP+I组心肌细胞Caspase-3活性增高(P<0.05或P<0.01).结论 异丙酚可通过上调HO-1的表-达而减轻H_2O_2导致的心肌细胞损伤.

Effects of Propofol on the Heme Oxygenase-1 Expression in Rats with H_2O_2-mediated Damage to Cultured Cardiac Myocytes

Objective To investigate the effect of propofol on the heme oxygenase-1(HO-1)expression in rats with H_2O_2-mediated damage to cultured cardiac myocytes.Methods Primary cultured new-born rat cardiac myocytes were divided into 8 groups:control,H_2O_2 group,low dose propofol (LP) group,middle dose propofol(MP)group,high dose propofol(HP)group,LP +ZnPP Ⅸ group.MP+ZnPP Ⅸ group and HP+ZnPP Ⅸ group.The cells in all groups were incubated for 6 h.The concentration of malondialdehyde(MDA),activity of superoxid dismuase(SOD),mitochondria and Caspase-3,and the expression of HO-1 were determined.Results As compared with H_2O_2 group,the HO-1 expression,and the activity of SOD and mitochondria were significantly increased(P<0.05,P<0.01),and activity of Caspase-3 and concentration of MDA was decreased(P<0.05)in MP and HP groups.As compared with LP,MP and HP groups respectively.the HO-1 expression and SOD activity were significantly decreased and the concentration of MDA increased in LP+ZnPP IX,MP+ZnPP Ⅸ and HP+ZnPP Ⅸ groups(P<0.05,P<0.01),while Caspase-3 activity was significantly increased in MP+ZnPP IX and HP+ZnPP IX(P<0.05,P<0.01).Conclusion Propofol can protect cardiac myocytes against H_2O_2-mediated cytotoxicity in a dose-dependent manner,and increase the HO-1 expression,which may partly mediate cytoprotective effects of propofol.