黄芩苷元对心肌缺血再灌注损伤大鼠心肌能量代谢及NO和细胞凋亡的影响  

Effects of baicalein on energy metabolism,nitric oxide and apoptosis of myocardial ischemia-reperfusion injury in rats

作　　者：黄贤华[1] 刘宗亮[1] 刘贤伟[1] 郑建锋[1] 黄常亮[1] 邓文龙[2] 杨芳炬[3] 

机构地区：[1]赣南医学院,赣州341000 [2]四川省中医药科学院,成都610041 [3]四川大学华西医学中心药理教研室,成都610041

出　　处：《中药药理与临床》2009年第5期34-37,共4页Pharmacology and Clinics of Chinese Materia Medica

基　　金：国家重点基础研究发展计划(2007CB512604)

摘　　要：目的:观察黄芩苷元(Baicalein,Bai)对大鼠心肌缺血再灌注损伤的保护作用,并进一步探讨其作用机制。方法:结扎大鼠左冠状动脉前降支以制备心肌缺血再灌注损伤模型,比色法检测大鼠心肌匀浆中钠-钾-三磷酸腺苷酶(Na+-K+-ATPase)、钙-三磷酸苷酶(Ca++-ATPase)、乳酸(LD)和一氧化氮(NO)含量;显微镜下观察心肌坏死程度;免疫组织化学方法检测Bcl-2与Bax蛋白在心肌细胞上的表达,并计算Bcl-2/Bax的比值。结果:与模型组比,Bai能提高心肌中Na+-K+-ATPase、Ca++-ATPase活性,增加NO含量,降低心肌中LD含量;减少Bax蛋白表达,提高Bcl-2/Bax的比值。结论:Bai对心肌缺血再灌注损伤大鼠有保护作用,作用机制可能与其改善心肌能量代谢和抗凋亡等作用有关。Objective：To investigate protective effects of baicalein in myocardial ischemia-reperfusion injury rats.Methods： To establish the myocardial ischemia-reperfusion injury model in rats by ligating left anterior descending coronary artery.The content of Na＋-K＋-ATPase,Ca＋＋-ATPase,lactic acid and nitric oxide in myocardium were measured by chromato-metry;The degree of myocardiolysis was observed by microscope;The express of Bcl-2 and Bax proteins in myocardium were measured by immunohistochemistry,and the ratio of Bcl-2/Bax proteins was calculated.Results： Experiment results in vivo showed that baicalein could significantly increase Na＋-K＋-ATPase,Ca＋＋-ATPase and nitric oxide contents,reduce lactic acid content in myocardium.baicalein could also reduce the expression of Bax proteins in myocardium and increase ratio of Bcl-2/Bax proteins.Conclusions：Baicalein exerts protective effect on myocardial ischemia-reperfusion injury in rats by improving energy metabolism and inhibiting the apoptosis of myocardial cells.

关 键 词：黄芩苷元 心肌缺血 再灌注损伤 

分 类 号：R285.5[医药卫生—中药学]