【摘要】 目的:探讨银杏叶提取物(EGB)对缺血心肌的细胞保护机制。方法:用垂体后叶素(20u/kg,ip)复制小鼠急性心肌缺血模型,观察不同剂量(100、200mg/kg)EGB对心肌缺血60min线粒体获得率,膜磷脂含量,Ca2+-ATP酶、Mg2+-ATP酶活性,MDA及胞浆SOD活性变化的影响。结果:预先给予EGB可有效抑制缺血所致线粒体膜磷脂含量减少,MDA水平增高,提高线粒体Ca2+-ATP酶及胞浆SOD酶活性,其部分作用表现为剂量依赖性。结论:EGB对缺血心肌的保护作用可能与其增加胞液SOD活性,防止线粒体膜脂质过氧化,维持线粒体膜Ca2+-ATP酶活性,改善缺血心肌2+细胞Ca转运有关。更多还原

【Abstract】 Objective:To understand the cell protective effects of Extracts from leaves of Ginkgo biloba(EGB) on the ischemic myocardium and evaluate its mechanism. Methods:On the mice myocaerdial ischemia model induced by pituirin (20u/kg,ip),the mitochondria membrane phospholipids contents,the yield rat of mitochondria fractions, Ca2+-ATPase activity, Mg2+-ATPase activity, MDA contents as well as SOD activity in cytoplasm were determined in control, ischemic and EGB groups. Results:EGB was able to enhance the mitochondial membrane phospholipids contents, Ca2+-ATPase activity, and SOD activity and to decrease the MDA level in ischemic myocardium. Conclusions:EGB can effectively protect ischemic myocaldium. The protecting mechanism of EGB on ischemic myocardium may be relate to strongly inhabit the lipide peroxidative damage, decrease the MDA levels, inhance superoxide dismutase(SOD) and Ca2+-ATPase activity, improve the mitochondrial Ca2+- transport function in ischemic myocardium.更多还原