氧自由基在心肌保护第二窗中的作用

Role of Oxygen Free Radicals in the Second Window of Myocardial Protection

目的：证实短暂、重复缺氧后即刻产生的氧自由基是否诱导了２４小时后心肌抗氧化酶等保护蛋白增加而引起心肌延迟保护。 方法：在大鼠培养心肌细胞缺氧预适应模型上，设正常对照组、缺氧复氧组、缺氧预适应组、外源性超氧阴离子处理组（外源性Ｏ２处理组）和超氧化物歧化酶处理组（ＳＯＤ处理组），用酶联免疫吸附试验法检测预适应后即刻和２４小时末心肌细胞外源性超氧阴离子（ＯＦ）的产生量、热休克蛋白７２（ＨＳＰ７２）表达及一氧化氮合酶（ＮＯＳ）活性、超氧化物歧化酶（ＳＯＤ）、谷胱甘肽和丙二醛含量及心肌细胞存活率。 结果：与正常对照组比较，缺氧预适应后即刻Ｏ２产生量在缺氧预适应组和外源性Ｏ２处理组升高，有非常显著性差异（Ｐ＜０．０１），缺氧复氧组和ＳＯＤ处理组无显著变化，相反，缺氧预适应后２４小时前２组Ｏ２的产生量较缺氧复氧组和ＳＯＤ处理组显著减少，有非常显著性差异（Ｐ＜０．０１），且与正常对照组比较无显著性差异（Ｐ＞０．０５）。且前２组ＨＳＰ７２和ＳＯＤ比后２组增加，有非常显著性差异（Ｐ＜０．０１）；各组心肌细胞存活率、ＮＯＳ活性及谷胱甘肽均有不同程度下降，丙二醛有不同程度增加，但前２组各指标降幅和增幅分别较后２组小，有显著性差异（Ｐ?

Objective:To investigate whether oxygen free radicals (OFRs) generated immediately after brief,repeated hypoxia induce the increase of the myocardial protective proteins 24 hours later and lead to the late cardioprotection. Methods: In the model of anoxia preconditioning (APC), the productions of superoxide anion (O2-),expressions of heat shock protein 72 (HSP72), activity of nitric oxide synthase (NOS), and contents of antioxidant enzymes and cell viability were measured in the cultured myocardial cells of rats. Results: Immediately after APC, O2 production was significantly higher in the APC group and exogenous O2treated group (p＜０. 01),and no significant change in the anoxia /reoxygenation (A/R ) group and superoxide dismutase (SOD) treatment group than that in the control group,Reversely,at the end of A/R and SOD group after 24 hours,O2- production increased significantly (p＜0. 01),and no significarot change than contral group (p>0. 05),HSP72 and SOD increased significantly in the first two groups than in the late two groups (p<0. 01). In every group,malondiadehyde were obvious increased and cell viability,NOS and glutathione were remarkable decreased,but the degree of increase and decrease were lower in the first two groups than in the late two groups(p<0. 05). Immediately after APC,there was no difference between groups except O2- production(p>0. 05). Conclusion: OFRs can increase contents of antioxidant enzymes and induce the expressions of HSP72 and it contributes to the late cardioprotective.