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目的观察硫化氢(H2S)对大鼠心肌缺血再灌注损伤后的作用。方法采用大鼠在体结扎冠状动脉前降支30min后,松解扎扣后再灌注60min造成心肌缺血再灌注损伤模型,使用ELISA法测定心肌缺血再灌注前后大鼠心肌肌钙蛋白Ⅰ(cTnⅠ)水平,使用TUNEL法进行细胞凋亡检测,使用免疫组化法测定凋亡相关蛋白Caspase-3水平,测定所有动物测定血流动力学指标,各组观测缺血和梗死范围。结果在使用了硫氢化钠作干预的情况下大鼠的心肌肌钙蛋白明显较低,心肌的缺血和梗死范围也较对照组要小,在大鼠的心肌缺血再灌注损伤过程中H2S可显著降低心肌细胞Caspase-3的表达水平,从而减少心肌细胞的凋亡。结论 H2S在大鼠心肌缺血再灌注损伤过程中具有保护作用,其作用机制可能是通过减少缺血再灌注过程中心肌细胞的凋亡数量,从而起到对心肌的保护作用。
Objective To observe the effect of hydrogen sulfide (H2S) on myocardial ischemia-reperfusion injury in rats. Methods The rat anterior descending coronary artery was ligated for 30 minutes in vivo and then the myocardial ischemia-reperfusion injury model was induced by loosening and fastening and then reperfusion for 60 minutes. The levels of cardiac troponin Ⅰ cTnⅠ) were detected by immunohistochemical method. Apoptosis was detected by TUNEL method. Caspase-3 level was detected by immunohistochemistry. All animals were measured for hemodynamic parameters. The ranges of ischemia and infarction were observed in all groups. Results In the case of intervention with sodium hydrosulfide, cardiac troponin in rats was significantly lower, myocardial ischemia and infarct size than the control group is smaller, in the process of myocardial ischemia-reperfusion injury in rats H2S Can significantly reduce the expression of Caspase-3 in cardiomyocytes, thereby reducing the apoptosis of cardiomyocytes. Conclusions H2S may play a protective role in the process of myocardial ischemia-reperfusion injury in rats. The possible mechanism is that H2S may play a protective role on myocardium by decreasing the number of apoptotic cardiomyocytes during ischemia-reperfusion.