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目的:观察促红细胞生成素(erythropoietin,EPO)对大鼠心肌缺血再灌损伤的影响,并探讨机制。方法:以左冠状动脉前降支(LAD)穿线结扎法制备心肌缺血模型,松开结扎线造成再灌注。45只SD大鼠随机分成5组:①假手术组,②缺血再灌注组,③磷脂酰肌醇-3-激酶(PI3K)的高选择性阻断剂LY294002组,④EPO组和⑤EPO+LY294002组。观察心电图Ⅱ导联心律失常发生情况,进行室性心律失常评分;电镜观察心肌细胞超微结构;以TUNEL法检测细胞凋亡;检测血清肌酸磷酸激酶同工酶(CK-MB)和肌钙蛋白I(cTnI)水平。结果:EPO能降低心律失常评分(P<0.01),减轻心肌细胞超微结构损伤,减少细胞凋亡(P<0.01),降低血清CK-MB和cTnI水平(P<0.01),但这些作用可被预先给予的LY294002所减弱。结论:EPO能减轻心肌缺血再灌注损伤,PI3K参与其信号转导。
Objective: To observe the effect of erythropoietin (EPO) on myocardial ischemia-reperfusion injury in rats and its mechanism. Methods: The model of myocardial ischemia was created by ligating the left anterior descending coronary artery (LAD), releasing the ligature and reperfusion. 45 SD rats were randomly divided into 5 groups: ① sham operation group, ② ischemia reperfusion group, ③ phosphatidylinositol 3-kinase (PI3K) highly selective blocker LY294002 group, ④ EPO group and ⑤ EPO + LY294002 group. The incidence of arrhythmia in ECG Ⅱ was observed and the ventricular arrhythmia was evaluated. The ultrastructure of myocardial cells was observed by electron microscope. The apoptosis was detected by TUNEL method. Serum levels of CK-MB and CK Protein I (cTnI) levels. Results: EPO decreased the arrhythmia score (P <0.01), reduced the myocardial ultrastructure damage, decreased the apoptosis (P <0.01) and decreased the levels of CK-MB and cTnI in serum (P <0.01) Weakened by pre-given LY294002. Conclusion: EPO can reduce myocardial ischemia-reperfusion injury and PI3K participate in signal transduction.