黑木耳多糖对抗大鼠慢性缺血性心肌损伤  

Effect of Auricularia auricular polysaccharide on ischemia myocardial injury

作　　者：叶挺梅[1] 崔洁[2] 钱令波[2] 王会平[2] 叶治国[2] 夏强[2] 

机构地区：[1]丽水学院化学与生命科学院生物系,浙江丽水323000 [2]浙江大学医学院生理学教研室,浙江杭州310058

出　　处：《中国病理生理杂志》2009年第11期2118-2121,共4页Chinese Journal of Pathophysiology

基　　金：浙江省科技厅基金资助项目(No.2006C23040)

摘　　要：目的:在整体大鼠心脏冠脉结扎模型上研究黑木耳多糖(AAP)的心肌保护作用,并探讨其作用机制。方法:在体大鼠实验模型,结扎冠状动脉左前降支,测定心肌梗死面积、血清乳酸脱氢酶(LDH)含量、超氧化物歧化酶(SOD)的活性、丙二醛(MDA)的含量以及心肌纤维化程度,观察不同剂量的黑木耳多糖(50、100和200mg·kg-1.d-1,共20d)的心肌保护作用,复方丹参作为阳性对照。结果:黑木耳多糖灌胃可明显减小在体大鼠缺血心肌的梗死面积,降低血清中LDH的含量。黑木耳多糖可明显减少MDA的生成,增强SOD活性,使心肌胶原纤维蛋白的含量降低。结论:黑木耳多糖能对抗大鼠缺血性心肌损伤,其机制可能与其抗氧化作用有关。AIM： To investigate the protective effect of auricularia auricular polysaccharide （AAP） on the myocardial injury induced by ischemia and its underlying mechanism. METHODS： AAP was orally administrated to rats at the does of 50, 100 or 200 mg ·k^-1·d^-1 for 20 d. Myocardial injury was induced in anesthetized Sprague -Dawley rats by left anterior descending coronary artery ligation. Myocardial infarct size, the level of lactate dehydregenase （LDH）, the activity of superoxide dismutase （SOD）, the production of lipid peroxidation malondialdehyde （MDA） and protein level of myocardial collagen of the heart were measured. RESULTS ： The average myocardial infarct size in AAP groups was significantly smaller than that in ischemia group. The level of serum LDH induced by regional myocardial ischemia was significantly decreased in AAP group compared to ischemia group （ P 〈 0. 01 ）. AAP inhibited the production of MDA and increased the activity of SOD. Furthermore, AAP reduced the protein level of myocardial collagen after ischemia （P 〈 0. 01 ）. CONCLUSION ： AAP prevents myocardium from isehemia injury as an antioxidant.

关 键 词：黑木耳多糖 心肌缺血 抗氧化 

分 类 号：R542.2[医药卫生—心血管疾病]