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目的探讨促红细胞生成素(erythropoietin,EPO)抑制心梗大鼠心肌核转录因子CHOP(C/EBP homologous protein)表达的作用。方法将雄性SD大鼠30只随机分为假手术对照组、心肌梗死组和EPO治疗组。心肌梗死组及心肌梗死EPO治疗组采用结扎左冠状动脉前降支建立心梗模型。其中EPO治疗组术后每天腹腔注射重组人促红细胞生成素(recombinant human erythropoietin,rh-EPO)(1 000 u.kg-1),其余2组注射等量生理盐水,30 d后,分别测定各组大鼠心功能,观察梗死区及其周围心肌病理改变,同时免疫组化和Western-blot方法测定并比较3组大鼠心梗区域心肌细胞核转录因子CHOP蛋白的表达改变。结果 EPO治疗组大鼠心功能较心肌梗死组大鼠明显改善,表现为左室发展压(left ventricular developed pressure,LVDP)值较梗死组大鼠升高,但比假手术对照组低(P<0.01),梗死组心肌纤维化严重,残存心肌排列紊乱,而EPO治疗组可见梗死心肌部位的间质纤维化明显改善。免疫组化和Western-blot显示实验组中核转录因子CHOP蛋白在EPO治疗组表达明显低于心肌梗死组(P<0.05)。结论 EPO可以明显改善心梗大鼠的心功能,其机制可能与抑制核转录因子CHOP的过表达从而抑制内质网应激引起的心肌细胞凋亡有关。
Objective To investigate the effect of erythropoietin (EPO) on the expression of C / EBP homologous protein (CHOP) in myocardial infarction rats. Methods Thirty male SD rats were randomly divided into sham-operation control group, myocardial infarction group and EPO-treated group. Myocardial infarction and myocardial infarction EPO treatment group was established by ligation of left anterior descending coronary artery. The EPO group was injected intraperitoneally with recombinant human erythropoietin (1 000 u.kg-1), and the other two groups were injected with the same amount of saline at the end of the experiment. After 30 days, The heart function of the rats was observed. The myocardial pathological changes were observed in infarct area and surrounding area. The expression of CHOP protein in myocardial infarction area was detected by immunohistochemistry and Western-blot. Results Compared with the sham operation group, the left ventricular developed pressure (LVDP) increased significantly in the EPO group than in the sham operation group (P < 0.01). Severe myocardial fibrosis was found in the infarcted group and the remnant myocardium was disordered. In the EPO group, interstitial fibrosis in the infarcted myocardium was markedly improved. Immunohistochemistry and Western-blot showed that the expression of CHOP in the experimental group was significantly lower than that in the myocardial infarction group (P <0.05). Conclusions EPO can significantly improve the cardiac function in myocardial infarction rats. The mechanism may be related to the inhibition of the overexpression of nuclear factor CHOP and the inhibition of endoplasmic reticulum stress-induced cardiomyocyte apoptosis.