黄芩甙对大鼠心肌缺血再灌注所致脂质过氧化损伤的保护作用  

Protective Effect of Baicalin on Lipid Peroxidation Induced by Myocardical Postischemic Reperfusion in Rats

作　　者：欧阳昌汉[1] 吴基良[1] 李立中[1] 

机构地区：[1]咸宁医学院药理学教研室,湖北咸宁437100

出　　处：《咸宁医学院学报》2001年第1期32-34,共3页Journal of Xianning Medical College

摘　　要：目的研究黄芩甙 (baicalin ,Bai)对大鼠心肌缺血再灌注所致脂质过氧化损伤的保护作用。方法采用结扎在体大鼠冠状动脉左前降支造成心肌缺血 30min ,随后恢复血流行再灌注 1 2 0min ,复制心肌缺血再灌注损伤模型。结果Bai能不同程度地降低缺血再灌注所引起心肌组织脂质过氧化物丙二醛(MDA)含量升高 ,提高超氧化物歧化酶 (SOD)活性 ,保护Na+ -K+ -ATP酶活力 ,降低血清肌酸激酶(CK)和乳酸脱氢酶 (LDH)水平。结论Bai可通过保护脑组织抗氧化酶的活性 ,抑制脂质过氧化反应 ,减轻自由基对心肌组织的损害 ,对缺血再灌注心肌产生保护作用。Objective To investigate the effects of baicalin on lipid peroxidation induced by myocardical ischemia reperfusion (I/R) in rats.Methods The experimental model was established by ligation of left anterior descending coronary artery for 30min followed by reperfusion for 120min in anaesthesized rats.Result Baicalin decreased the content of malonaldehyde(MDA),elevated the activity of superoxide dismutase(SOD),suspressed the reduction of Na +-K +-ATPase activity to certain extent in reperfusion myocardium;decreased lactate dehydrogenase(LDH) and creatine kinase(CK) level in serum in comparison with I/R group.Conclusion Baicalin have protective effects on myocardical postischemic reperfusion injury by enhancing the activity of auti oxidative enzyme subsequently inhibiting lipid peroxidation and attenuating the oxygen free radicals mediated damage to the myocardium.

关 键 词：黄芩甙 心肌缺血 再灌注损伤 NA^+-K^+-ATP酶 超氧化物歧化酶 丙二醛 脂质过氧化损伤 

分 类 号：R259.422[医药卫生—中西医结合] R285.5[医药卫生—中医内科学]