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益母草碱对急性心肌梗死大鼠的影响
引用本文:徐玉平,钱海兵,朱依谆. 益母草碱对急性心肌梗死大鼠的影响[J]. 中国实验方剂学杂志, 2016, 22(17): 113-116
作者姓名:徐玉平  钱海兵  朱依谆
作者单位:凯里学院, 贵州 凯里 556011;贵阳中医学院, 贵阳 550002,贵阳中医学院, 贵阳 550002,复旦大学, 上海 201203
基金项目:贵州省国际科技合作项目(黔科合外G字[2010]7012)
摘    要:目的:观察益母草碱对急性心肌梗死造成的心肌缺血和心肌细胞损害的影响并探讨其作用机制。方法:雄性SD大鼠随机分为5组,分别为假手术组,模型组,益母草碱高、低剂量组(30,15 mg·kg-1·d-1)和卡托普利阳性药组(4 mg·kg-1·d-1),除假手术组外其余各组采用结扎冠状动脉左前降支的方法制备大鼠急性心肌梗死模型,所有动物冠脉结扎前1周按相应剂量ip药物,第8天造模,术后继续ip给药2 d后,处死动物,2,3,5-氯化三苯基四氮唑(TTC)染色法检测并计算心肌梗死面积,酶联免疫吸附测定(ELISA)试剂盒测定大鼠血清中乳酸脱氢酶(LDH),肌酸激酶(CK)的水平,超氧化歧化酶(SOD)活性和丙二醛(MDA)含量。结果:与假手术组比较,模型组大鼠心肌梗死面积明显增大,血清中LDH,CK,MDA含量水平明显升高,总超氧化物歧化酶(T-SOD)水平明显降低(P0.05,P0.01);与模型组比较,益母草碱能明显减小心梗大鼠左心室梗死面积,并能明显降低心梗大鼠血清中LDH,CK及MDA的水平,明显升高血清中T-SOD的活性(P0.05,P0.01)。结论:益母草碱对急性心肌缺血造成的心肌损伤有良好的预防性保护作用,其作用机制可能与提高心肌组织抗氧化能力有关。

关 键 词:益母草碱  急性心肌梗死  心肌缺血  乳酸脱氢酶  肌酸激酶
收稿时间:2015-08-14

Effect of Leonurine on Rats of Acute Myocardial Infarction
XU Yu-ping,QIAN Hai-bing and ZHU Yi-zhun. Effect of Leonurine on Rats of Acute Myocardial Infarction[J]. China Journal of Experimental Traditional Medical Formulae, 2016, 22(17): 113-116
Authors:XU Yu-ping  QIAN Hai-bing  ZHU Yi-zhun
Affiliation:Kaili University, Kaili 556011, China;Guiyang College of Traditional Chinese Medicine, Guiyang 550002, China,Guiyang College of Traditional Chinese Medicine, Guiyang 550002, China and Fudan University, Shanghai 201203, China
Abstract:Objective: To study the effect of leonurine on myocardial ischemia and myocardial cell injury caused by acute myocardial infarction, and its functional mechanism. Method: The model of acute myocardial infarction in rats was established through ligation of the left anterior descending coronary artery. Male SD rats were randomly divided into five groups:sham-operated group, leonurine high-dose (30 mg · kg-1 · d-1) group, low-dose (15 mg · kg-1 · d-1) group, positive control group and model group. One week before the coronary artery ligation, all groups, except for the sham-operated group, were given the corresponding dose of drugs. The model was built on the eighth day, and postoperative intraperitoneal administration lasted for 2 days. The animals were sacrificed, and myocardial infarct size was measured by TTC staining. The content of lactate dehydrogenase (LDH), creatine kinase (CK), superoxide dismutase (SOD) and malondialdehyde (MDA) in rat serum were determined with enzyme-linked immuno sorbent assay (ELISA) kit. Result: Compared with the sham-operated group, the model group showed significant increase in myocardial infarct size, and serum LDH, CK and MDA content, and significant decrease in total superoxide dismutase (T-SOD) (P<0.05, P<0.01); compared with the model group, the leonurine group showed significant decrease in myocardial infarct size, and serum LDH, CK and MDA content, and significant increase in total superoxide dismutase (T-SOD) (P<0.05, P<0.01). Conclusion: Leonurine has a good protective effect on myocardial injury caused by acute myocardial ischemia. Its mechanism may be related to the improvement of the antioxidant capacity of myocardial tissues.
Keywords:leonurine  acute myocardial infarction  myocardial ischemia  lactate dehydrogenase  creatime kimase
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