冠心Ⅱ号抗缺血性心肌损伤的自由基机理实验研究

Study on Free Radical Mechanism of Guanxin Ⅱ in Antagonizing Ischemic Myocardial Damage

目的 :比较研究冠心Ⅱ号及其组成成分丹参、赤芍、川芎、红花、降香清除活性氧自由基 (OFR) ,克服实验性急性心肌缺血所致损伤及保护心肌组织的分子作用机制。方法 :大鼠腹腔注射垂体后叶素 (pit) ,致急性心肌缺血作为实验动物模型 ,采用低温电子顺磁共振 (EPR)技术直接测定动物组织内氧自由基的水平。结果 :模型组大鼠心肌组织的病理切片 (HE染色 )及通过大鼠心电图的描记证实心肌组织发生了急性心肌缺血的典型病变 ,EPR实验表明心肌组织内OFR水平异常增高 ;而冠心Ⅱ号及其各单味药的乙醇粗提物均可使心肌组织内异常的自由基水平降低或接近正常 ,因而减轻了心肌组织的损伤程度。结论 :氧自由基过量生成导致心肌组织损伤。运用低温EPR技术可直接测定其水平。冠心Ⅱ号及其组分抵抗并修复心肌损伤作用的分子机理之一是清除组织内异常增高的活性氧自由基。为进一步探讨中药复方的组方机理提供依据。

Objective: To study comparatively the effect of Guanxin Ⅱ and its constituents, including Salvia, Red Peony root, Chuanxiong, Safflower and Dalbergia wood, in scavenging active oxygen free radical (OFR) to explore their mechanism in overcoming the experimental acute ischemic myocardial injury and protecting myocardial tissue. Methods: The experimental acute myocardial ischemic model was established by intraperitoneal injection of pituitrin to rats. OFR level in animal heart tissue was directly measured with low temperature electron paramagnetic resonance (EPR) spectrometer. Results: The pathological examination of HE stained slide of myocardial tissue and electrocardiography of model animal showed that typical changes of acute myocardial ischemia occurred in myocardial tissue, EPR showed that OFR level in myocardial tissue increased abnormally. The ethanol extract of Guanxin Ⅱ and its constituents could lower the increased OFR level close to normal, thus to alleviate the myocardial damage. Conclusion: Overproduction of OFR could induce damage of heart tissue, its level could be measured directly using low temperature EPR. One of the molecular mechanisms of Guanxin Ⅱ and its constituents in antagonizing and repairing myocardial damage is to scavenge the abnormal increased active OFR in tissue. This study has provided a basis for further studying the mechanism of Chinese composite recipes and their constituents.