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 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.
出处
《辽宁中医杂志》
CAS
2012年第1期175-177,共3页
Liaoning Journal of Traditional Chinese Medicine
基金
国家自然科学基金(30572435)
江西省教育厅青年科学基金(GJJ09628)
