木棉花总黄酮对大鼠心肌缺血再灌注损伤的保护作用

目的 研究木棉花总黄酮对大鼠心肌缺血再灌注损伤的保护作用，并探讨其作用机制。方法 将健康SD大鼠随机分为假手术组、模型组、阳性对照组（复方丹参滴丸135 mg·kg^-1），木棉花总黄酮低、中、高剂量组（100，200，400 mg·kg^-1）。每日灌胃给药1次，连续给药7 d，假手术组与模型组每天灌服等体积的生理盐水，采用冠状动脉左前降支结扎法建立心肌缺血再灌注损伤模型，检测大鼠血清肌酸激酶同工酶（CK-MB）、肌酸激酶（CK）、乳酸脱氢酶（LDH）、乳酸脱氢酶同功酶1（LDH-1）、超氧化物歧化酶（SOD）、还原型谷胱甘肽（GSH）、谷胱甘肽过氧化物酶（GSH-Px）、丙二醛（MDA）、一氧化氮（NO）和一氧化氮合酶（NOS）的变化。TTC法测量心肌梗死面积，并观察心肌组织病理学变化。结果 与假手术组比较，模型组大鼠血清中CK-MB、CK、LDH、LDH-1、MDA的含量显著升高，SOD、GSH、GSH-Px、NO和NOS的活性显著降低，心肌组织严重梗死和坏死；与模型组比较，木棉花总黄酮各剂量组能明显降低大鼠血清中CK-MB、CK、LDH、LDH-1、MDA的含量，提高SOD、GSH、GSH-Px、NO和NOS的活性，同时可减少心肌梗死面积，减轻心肌细胞肿胀和炎性细胞浸润，改善缺血心肌的病理变化。结论 木棉花总黄酮对大鼠心肌缺血再灌注损伤有明显保护作用，其机制可能与减少氧自由基的产生，调节氧化与抗氧化平衡有关。

Protective Effect of Total Flavonoids of Gossampim Flos on Myocardial Ischemia and Reperfusion Injury in Rats

OBJECTIVE To study the protective effect of total flavonoids of Gossampim Flos(TFG) on myocardial ischemia and reperfusion injury in rats, and to explore its mechanism. METHODS Healthy SD rats were divided into six groups randomly, 10 rats in each group:sham operation group, model group, positive control group(composite salviae dropping pill 135 mg·kg^-1), TFG low-dose, middle-dose and high-dose group(100, 200, 400 mg·kg^-1), respectively. Except the sham operation group and model group, the rest of the groups were administrated with drugs by ig for 7 days, and once a day, the sham group and the model group were given normal saline. Myocardial ischemia reperfusion injury model was established by anterior descending branch of coronary artery. The activity of CK-MB, CK, LDH and LDH-1 in serum were measured, the levels of SOD, GSH, GSH-Px, NOS and the content of MDA, NO were detected, and myocardial infarct size was assessed by TTC staining, the myocardial tissue lesion was observed by histopathology. RESULTS Compared with the sham operation group, the serum levels of CK-MB, CK, LDH, LDH-1 and MDA were significantly increased in the model group, the activity of SOD, GSH, GSH-Px, NO and NOS in serum of rats in the model group was significantly reduced, myocardial tissue cells were severely infarcted and necrotic. Compared with model group, TFG could significantly reduce the serum contents of CK-MB, CK, LDH, LDH-1 and MDA in rats in each dose group, and could improve the activity of SOD, GSH, GSH-Px, NO and NOS, at the same time, the myocardial infarction area could be reduced, the light microscopic myocardial tissue edema levels and inflammatory cell infiltration were significantly lightened. CONCLUSION TFG shows remarkable protective effects on myocardial ischemia and reperfusion injury in rats, the mechanism may be related to reducing the production of oxygen free radicals and regulating oxidation and antioxidant balance.