中文摘要：

目的：研究缺血再灌注损伤心肌EPOR的表达和调控机制及丹参酮ⅡA的忏预作用。方法：实验大鼠随机分为假手术组、模型组、PDTC组，丹参酮ⅡA组。冠脉结扎和再松开复制动物模型，计算心律失常评分和心肌梗死面积，免疫组化法检测心肌组织EPOR、NF—κB的表达。结果：与假手术组比较，模型组EPOR、NF—κB的表达增强（P〈0．01）；PDTC和丹参酮ⅡA预处理后NF—κB的表达均显著减少（P〈0．01），而EPOR的表达均进一步增强（P〈0．01）。结论：心肌缺血再灌注损伤时EPOR的表达升高，抑制NF—κB介导的炎症反应可以进一步促进EPOR表达上调。丹参酮ⅡA也可以上调EPOR的表达，其机制可能与抑制NF—κB介导的炎症反应有关。

英文摘要：

Objective ： To study the expression of EPOR in ischemia - reperfusion injured myocardium and the regulation mechanism, and the intervention effect of tanshinone Ⅱ A. Methods ： Rats were randomly divided into four groups ： sham operation group, model group, PDTC group, tanshinone Ⅱ A group. Experimental animal model was conducted by ligating and loosening left anterior descending coronary. Arrhythmia score, infarct size, and the expression of EPOR and NF - κB were compared in the three groups. The expressions of EPOR and NF - κB were determined by immunohistoehemical staining. Results ： The expressions of EPOR and NF - κB in model group were significantly higher than that in sham operation group （P 〈 0.01） , and the expression of NF - κB was significantly decreased after the pretreatment of PDTC or tanshinone Ⅱ A,while the expression of EPOR increased significantly （P 〈 0.01 ）. Conclusion：Myocardial ischemia - reperfusion injury could lead to high expression of EPOR, inhibit the expression of NF - κB and enhance the expression of EPOR. Tanshinone Ⅱ A could regulate the expression of EPOR,its mechanism may be related to prevention of the inflammatory reaction induced by NF - κB.