黄蜀葵花总黄酮对心肌损伤的保护作用及其机制

目的　观察黄蜀葵花总黄酮对抗心肌损伤的保护作用及其机制。方法　观察黄蜀葵花总黄酮对用心电图ECG(LⅡ )记录注射垂体后叶素的大鼠心电图T波升高的幅度变化值 ;对冠状动脉结扎造成的急性心肌梗塞大鼠血清中CPK、LDH和血清游离脂肪酸水平的改变 ;对小鼠心肌线粒体中MDA、SOD和GSHPx的改变。结果　黄蜀葵花总黄酮(10 0 ,2 0 0mg·kg-1,ip)对注射垂体后叶素的大鼠心电图T波升高有抑制作用。对冠状动脉结扎造成的急性心肌梗塞大鼠 ,黄蜀葵花总黄酮 (10 0mg·kg-1·d-1× 3,ip)能够显著抑制血清中CPK、LDH的升高 ,降低血清游离脂肪酸水平。黄蜀葵花总黄酮 (5 0 ,10 0mg·kg-1·d-1× 3 ,ip)可以降低急性心肌梗塞大鼠的梗塞面积。黄蜀葵花总黄酮 (3mg·10g-1·d-1× 3 ,ip)对小鼠心肌线粒体中MDA的生成有抑制作用 ,也能提高SOD和GSHPx的活力。结论　提示黄蜀葵花总黄酮对心肌损伤有一定的保护作用 ,其作用机制可能部分在于对Mit的功能稳定及抗脂质过氧化 ,减少自由基生成相关

Protective effects and mechanism of total flavone of the flowers of Abelmoschl on the injury of myocardial ischemia

AIM To study the protective and mechanism of Tfa (total flavone of the flowers of Abelmoschl Manihot L. Medic). METHODS The rats were injected Iso and then the T wave movement value observed. The rats anterior descenging bracnch of left artery were occluded for 48 hours the results of CPK, LDH and disscoate fatty acid of serum and infarct area of myocardium observed. RESULTS Tfa 100,200 mg·kg -1 ,ip depressed the T wave rise by injection of Iso in rats. Tfa 100 mg·kg -1 ·d -1 ×3,ip inhibited the serum CPK and LDH disscoate fatty acid in myocardium induced by coronary artery occluded in rats;also markedly depressed the infarct area in myocardial infarct rats. Tfa 0 03 mg·kg -1 ·d -1 ×3,ip obviously reduced the MDA contents,increased SOD and GSHPx activities in the mitochondria in mice. CONCLUSION Tfa shows a protective effect against myocardial injury. The mechanism may be via against oxygen free radicals and lipid peroxidation,also stabilize the mitochondria function.