论文部分内容阅读
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的干预作用。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-КB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。
OBJECTIVE: To investigate the expression and regulation of EPOR in ischemia-reperfusion myocardium and the intervention of tanshinone IIA. Methods: The rats were randomly divided into sham operation group, model group, PDTC group and tanshinone IIA group. Coronary ligation and re-release of the animal model of replication, arrhythmia score and myocardial infarction area, immunohistochemical detection of myocardial tissue EPOR, NF-κB expression. Results: The expression of EPOR and NF-κB in model group were significantly increased (P <0.01), while the expression of NF-κB in PDTC and Tanshinone IIA group was significantly decreased (P <0.01) Further increased (P <0.01). Conclusion: The expression of EPOR is increased during myocardial ischemia-reperfusion injury. Inhibition of NF-КB-mediated inflammatory response may further promote the upregulation of EPOR. Tanshinone IIA can also up-regulate the expression of EPOR, the mechanism may be related to inhibition of NF-κB-mediated inflammatory response.