摘要
目的:研究中药有效成分黄芩苷(baicalin)对大鼠心肌缺血再灌注损伤的作用及其机制。方法:雄性Wistar大鼠随机分为4组,假手术组、对照组和黄芩苷50,100 mg·kg^(-1)组。结扎大鼠左冠状动脉前降支30 min后松开结扎线120 min复制心肌缺血-再灌注损伤模型,以多道生理记录仪持续记录左室压力变化速率(±dp/ dt_(max))和左室舒张末期压(LVEDP)的变化。检测心肌丙二醛(MDA)含量、超氧化物歧化酶(SOD)、Na^+-K^+-ATP酶和Ca^(2+)-ATP酶活性以及血清乳酸脱氢酶(LDH)和磷酸肌酸激酶(CK)含量,以透射电镜观察心肌超微结构的改变。结果:与假手术组比较,对照组大鼠左室±dp/dt_(max)明显降低(P<0.01),而LVEDP明显升高(P<0.01)。静脉注射黄芩苷50,100 mg·kg^(-1)可使降低的±dp/dt_(max)明显升高(P<0.05,P<0.01),升高的LVEDP显著降低(P<0.05,P<0.01)。黄芩苷组血清CK和LDH含量分别是(72±19)kU·L^(-1),(64±15)kU·L^(-1)和(1 365±209)U·L^(-1),(1 124±169)U·L^(-1),均明显低于对照组[(90±23)U·L^(-1)和(1 826±123)U·L^(-1),P<0.01]。对照组大鼠心肌SOD,Na^+-K^+-ATP酶和Ca^(2+)-ATP酶活性均明显低于假手术组,而降低的酶活性可被预先给予黄芩苷所升高(P<0.05,P<0.01)。此外,黄芩苷还可降低缺血心肌MDA含量,改善心肌超微结构。结论:黄芩苷通过清除氧自由基,抗脂质过氧化,改善心肌ATP酶活性而保护心肌缺血再灌注损伤。
AIM: To study the protective ettects of baicalin on myocardial ischemia-reperfusion injury in rats. METHODS: The models of myocardial isehemia-reperfusion injury were established by occluding left anterior descending coronary artery (LAD) for 30 min, followed by reperfusion for 120 min. The rate of rise and decline of left ventrieular pressure (±dp/dtmax) and end-diastolic pressure of left ventricle (LVEDP) were monitored continuously with polygraph. After reperfusion, the blood and myocardium samples were taken for determination of malondialdehyde (MDA) content, superoxide dismutase (SOD), Na^+-K^+-ATPase, Ca^2+-ATPase activities in myocardium, creatine kinase (CK) and lactate dehydrogenase (LDH) in serum with speetrophotometer. The ultrastmetural changes in ischemie myoeardium were assessed by transmission electron microscope. RESULTS: Compared with control group, baiealin treatment with 50 mg·kg^-1 and 100 mg·kg^-1 depressed the changes in ± dp/ dtmax and LVEDP, decreased plasma CK and LDH levels, reduced myocardial MDA content, and increased the activities of SOD, Na^+-K^+-ATPase, and Ca^2+-ATPase in myocardium following ischemia-reperfusion. The uhrastmctural injury in reperfused myoeardium was relieved. CONCLUSION: Baiealin possesses a protective effect against myocardial isehnemia-reperfusion injury through scavenging oxide radicals and improving Na^+-K^+-ATPase and Ca^2+- ATPase activities.
出处
《中国新药与临床杂志》
CAS
CSCD
北大核心
2006年第6期407-412,共6页
Chinese Journal of New Drugs and Clinical Remedies
关键词
黄芩苷
心肌缺血
再灌注损伤
腺苷三磷酸酶
心室功能
肌酸激酶
乳酸脱氢酶
baicalin
myocardial ischernia
reperfusion injury
adenosine triphosphatase
ventricular function
creatine kinase
lactate dehydrogenase