布渣叶总黄酮对大鼠急性心肌缺血的保护作用及其机制

目的 研究布渣叶总黄酮对盐酸异丙肾上腺素注射液（ISO）诱导的急性心肌缺血大鼠模型的保护作用及其机制。方法 布渣叶总黄酮（8、4、2 mg/kg）每天ig给予大鼠1次，连续给药5 d，末次给药后1 h，ISO（2 mg/kg）多点sc诱导大鼠急性心肌缺血，观察布渣叶总黄酮对大鼠不同时间点心电图及心肌组织形态学的影响；生化法检测血清中乳酸脱氢酶（LDH）、肌酸激酶（CK）活性和心肌组织中超氧化物歧化酶（SOD）、丙二醛（MDA）和谷胱甘肽过氧化物酶（GSH-Px）水平。结果 与模型组相比，布渣叶总黄酮高、中剂量（8、4 mg/kg）组能明显对抗心肌缺血时心电图J点的下移（P＜0.05），尤以注射ISO后10 min时的效果较明显；明显改善ISO引起的心肌病理损伤；降低血清中LDH、CK水平（P＜0.05）和心肌组织 MDA的量（P＜0.01），提高心肌组织SOD（P＜0.01）和GSH-Px活性（P＜0.05、0.01）。结论 布渣叶总黄酮对大鼠急性心肌缺血损伤有明显的保护作用，其机制可能与提高心肌的抗氧化能力、减轻氧化应激反应有关。

Protection of total flavones from Microcos paniculata on acute myocardial ischemia in rats and its mechanism

Objective To study the protective effect of the total flavones in Microcos paniculata (TFMP) on the acute myocardial ischemia (AMI) induced by isoprenaline (ISO) and its mechanism. Methods The rats were ig administered with TFMP (8, 4, and 2 mg/kg) once daily for consecutive 5 d, and the AMI rat model was established by sc injection with ISO (2 mg/kg) 1 h after the last administration. The effects of TFMP on the electrocardiogram (ECG) at different time points and the myocardial tissue pathological histomorphology dying by hematoxylin were observed; The superoxide dismutase (SOD) and malondialdehyde (MDA) levels of myocardial tissue, glutathione peroxidase (GSH-Px), lactate dehydrogenase (LDH), and creatine kinase (CK) activities in serum were detected using biochemical method. Results Compared with the model group, the high- and mid-doses (8 and 4 mg/kg) TFMP inhibited the J spot downward of ECG during myocardial ischemia (P < 0.05), especially after 10 min of ISO injection. The myocardial injury induced by ISO was aslo improved in these two groups , the levels of LDH and CK in serum (P < 0.05) and the content of MDA in myocardial homogenate (P < 0.01) were decreased, the activities of SOD (P < 0.01) and GSH-Px (P < 0.05, 0.001) in the myocardial homogenate were increased. Conclusion The TFMP has the apparent protective effect on AMI injury, its mechanism may be related with improving the myocardial anti-oxidative ability and decreasing the oxidative stress reaction.