牡荆素对大鼠实验性心肌缺血损伤的保护作用及其机制

目的 研究牡荆素对实验性心肌缺血大鼠心肌损伤的保护作用及对其能量代谢的影响。方法 采用在体结扎大鼠心脏冠状动脉前降支法及舌下iv给予垂体后叶素（Pit）法建立大鼠心肌缺血损伤模型。在体大鼠缺血再灌注模型上，TTC染色法检测大鼠心肌梗死面积，并测定大鼠血清乳酸脱氢酶（LDH）和肌酸激酶（CK）活性；Pit致大鼠心肌缺血损伤模型上，检测大鼠心电图（ECG）、血清中LDH、CK、超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GSH-Px）活性及大鼠心肌组织中ATP酶活性，并观察大鼠心肌组织病理学改变。结果 牡荆素6、3、1.5 mg/kg可显著降低大鼠心肌梗死面积（P＜0.05、0.01），并能不同程度地降低血清中LDH和CK的活性。注射Pit后，模型组大鼠各时间点ECG的ST段变化值与对照组比较显著升高（P＜0.01）；葛根素与牡荆素（6、3 mg/kg）能显著降低Pit致大鼠心肌缺血升高的ST段（P＜0.05、0.01）。牡荆素（6、3 mg/kg）降低血清中LDH和CK的活性（P＜0.05、0.01），同时升高血清中SOD及GSH-Px的活性（P＜0.05、0.01）；牡荆素6、3、1.5 mg/kg和葛根素能明显升高缺血心肌组织中Na⁺, K^＋-ATP酶，Ca²⁺, Mg²⁺-ATP酶及总ATP酶的活性（P＜0.05、0.01）。牡荆素（6、3 mg/kg）可明显改善缺血心肌的病理损伤程度。结论 牡荆素对大鼠急性心肌缺血损伤具有明显保护作用，其作用与提高心肌组织抗氧化能力，改善心肌能量代谢有关。

Effect of vitexin on energy metabolism of experimental rats with myocardial ischemia and protective mechanism

Objective To study the mechanism of energy metabolism and protective effect of vitexin on experimental rats with myocardial ischemia(MI). Methods The MI model was made by occluding the left anterior descenging (LAD) of the coronary artery and induced by iv injection of high dose pituitrin(Pit) in rats. The areas of myocardial infarction were observed by tetrazolium chloride (TTC) staining, and the activities of lactate dehydrogenase (LDH) and creatine kinase (CK) in the serum were measured in rats on the myocardial infarction model by occluding LAD. The changes of ST wave at different time were determined by electrocardiogram (ECG), and the activities of LDH, CK, superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px) in the serum, and the activities of ATPase in tissue were measured in rats on the MI model induced by Pit. The pathological change of myocardium was observed. Results On the myocardial infarction model by occluding LAD in rats, vitexin (6, 3, and 1.5 mg/kg) significantly reduced the areas of myocardial infarction, and obviously reduced the activities of LDH and CK. On the MI model induced by Pit in rats, vitexin (6 and 3 mg/kg) markedly decreased the elevation of segment ST of ECG (P<0.05, 0.01), reduced the activities of LDH and CK, and increased the activities of SOD and GSH-Px in the serum of rats (P<0.05, 0.01). Vitexin (6, 3, and 1.5 mg/kg) significantly increased the activity of ATPase in the myocardium of rats (P<0.05, 0.01). Vitexin (6 and 3 mg/kg) improved myocardial pathologic alternation. Conclusion Vitexin exerts significant cardioprotective effects against acute ischemic myocardial injury in rats, likely that it could enhance anti-oxygen capability and improve energy metabolism in myocardial cells.