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目的观察地奥心血康(DAXXK)对大鼠心肌缺血再灌注(IR)损伤的保护作用和作用机制。方法采用大鼠心肌缺血再灌注损伤模型,观察DAXXK不同剂量组心肌缺血再灌注损伤所致ECG的ST段变化、心律失常出现和持续时间、心律失常评分、心肌梗死面积和心肌形态学指标的变化。TUNEL法检测心肌细胞凋亡,免疫组化法检测凋亡相关蛋白Fax、FasL表达情况,比色法测定心肌组织抗氧化能力,RT-PCR法检测心肌Mn-SODmRNA表达,ELISA法检测血管内皮分泌功能。结果与模型组相比,DAXXK各组,ECG中ST段抬高幅度显著降低,心律失常评分明显降低,心律失常发生的开始时间明显推后,持续时间明显缩短,心肌梗死面积明显缩小,心肌细胞肿胀和炎性细胞浸润减少,心肌细胞凋亡减少,心肌总超氧化物歧化酶(T-SOD)活力增强,Mn-SODmRNA表达增加,血管内皮功能改善。上述作用呈剂量依赖性。结论DAXXK对大鼠心肌缺血再灌注损伤的保护作用与其抗氧化损伤、抑制心肌细胞凋亡以及改善血管内皮功能有关。
Objective To observe the protective effect and mechanism of DAXXK on myocardial ischemia-reperfusion (IR) injury in rats. Methods The model of myocardial ischemia reperfusion injury in rats was used to observe the change of ST segment, the appearance and duration of arrhythmia, the arrhythmia score, the area of myocardial infarction and the morphological changes of myocardium caused by myocardial ischemia-reperfusion injury in DAXXK group The change. The apoptosis of cardiomyocytes was detected by TUNEL, the expression of apoptosis related protein Fax and FasL was detected by immunohistochemistry, the myocardial antioxidant capacity was measured by colorimetry, the expression of Mn-SOD mRNA was detected by RT-PCR, the secretion of vascular endothelial Features. Results Compared with the model group, the amplitude of ST elevation in ECG was significantly decreased and the arrhythmia score was significantly decreased in DAXXK groups. The onset time of arrhythmia was significantly delayed, the duration was significantly shortened, the area of myocardial infarction was significantly reduced, and myocardial cells Swelling and infiltration of inflammatory cells decreased, myocardial apoptosis decreased, myocardial SOD activity increased, Mn-SODmRNA expression increased, vascular endothelial function improved. The above effects were dose-dependent. Conclusion The protective effect of DAXXK on myocardial ischemia-reperfusion injury in rats is related to its anti-oxidative injury, inhibition of myocardial cell apoptosis and improvement of vascular endothelial function.