黄蜀葵花总黄酮对心肌缺血再灌注损伤的保护作用研究

目的：探讨黄蜀葵花总黄酮对大鼠心肌缺血再灌注损伤的保护作用。方法：采用犬鼠心肌缺血30min后再灌3．5h造成心肌缺血再灌注损伤模型，观察了黄蜀葵花总黄酮对损伤大鼠血清中CPK及心肌组织中MDA，SOD生成的影响；对培养的乳鼠心肌细胞采用缺糖缺氧和缺氧再给氧造成心肌细胞损伤观察黄蜀葵花总黄酮对LDH形成的影响；并采用TUNEL法分析细胞凋亡和采用免疫组化的方法观察药物对与心肌凋亡相关的蛋白Bcl-2表达的影响并阐述药物可能的作用机制。结果：黄蜀葵花总黄酮可以降低损伤心肌组织的MDA含量。提高SOD的活力，抑制血清中CPK的生成，也可以剂量依赖性抑制LDH的释放；减少心肌细胞凋亡的发生率，增强Bcl-2蛋白的表达。结论：黄蜀葵花总黄酮对心肌缺血再灌注损伤有保护作用，其作用机制部分可能与抗氧自由基的形成从而抑制细胞凋亡有关。

Protective Effects of Total Flavone from the Flowers of Ablemoschl manihot L. Medic on the Myocardial Ischemia/Reperfusion Injury

Object:To study the effects and mechanism of total flavone from the flowers of Ablemoschl Manihot L.Medic(Tfa) against myocardium injury induced by ischemia and reperfusion.Methods:The ischemia-reperfusion model was induced by after 30 min of coronary occlusion followed by 3.5 h of reperfusion in rats.The creatine phosphokinase(CPK) of serum,the malondialdehyde(MDA) and the superoxide dismutase(SOD) of myocardium were measured.The cell injure model in the cultured neonatal rat cardiomyocytes was induced by anoxia-reoxygenation and remove oxygen and glucose from medium,and the lactate dehydrogenase(LDH) was detected.Apoptosis was determined by terminal deoxy-nucleotidyl transferase-mediated dUTP-digoxigenin nick end-labeling(TUNEL) method and Bcl-2 expression determined by immunohistochemistry method.Results:The results showed that Tfa can decreased the MDA contents in myocardium and the production of CPK in serum,improved the SOD activitie;also decreased the number of apoptotic cells and enhanced the Bcl-2 expression in injured rat myocardium by ischemia/reperfusion.Tfa showed it can reduced the release of LDH from injured cardiomyocytes.Conclusion:Tfa showed the protective effect against myocardial ischemia and reperfusion injured which might be resist the damaging of oxygen free radical(OFR) and inhibited cardiomyocyte apoptosis.