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作 者:范一菲[1] 王云海[2] 张建华[3] 陈志武[3]
机构地区:[1]安徽医科大学生理学教研室,安徽合肥230032 [2]安徽医科大学第一附属医院普胸外科,安徽合肥230032 [3]安徽医科大学药理学教研室,安徽合肥230032
出 处:《中草药》2008年第2期240-244,共5页Chinese Traditional and Herbal Drugs
基 金:安徽省科技攻关重点资助项目(0613059A);安徽医科大学科研基金资助项目(2005Z031)
摘 要:目的观察杜鹃花总黄酮(TFRS)对大鼠心肌缺血再灌注损伤的保护作用及其机制。方法采用在体结扎大鼠心脏冠状动脉左前降支法,观察心电图ST段和T波的变化,TTC染色法测定心肌梗死面积并测定大鼠血清乳酸脱氢酶(LDH)、肌酸激酶(CK)活性,血清丙二醛(MDA)及一氧化氮(NO)水平,并应用逆转录酶链式反应(RT-PCR)方法测大鼠心肌中诱导型一氧化氮合酶(iNOS)mRNA表达情况。结果TFRS100mg/kg对缺血30min时ST段的抬高有明显抑制作用,TFRS25、50、100mg/kg对再灌注30min时ST段的抬高有明显抑制作用;TFRS50mg/kg能显著的降低心肌梗死面积;TFRS50、100mg/kg能不同程度降低血清中的LDH、CK的活性。TFRS50mg/kg可降低血清中MDA的水平;TFRS100mg/kg能显著提高心肌iNOSmRNA的表达。结论TFRS对心肌和缺血再灌注损伤有一定的保护作用,其作用机制可能与抗自由基和提高心肌iNOS基因mRNA的表达及增加NO产生有关。Objective To study the protective effect of total flavone trom Rhododendron strnsii (TFRS) on myocardial ischemia-reperfusion injury rats and its mechanism. Methods The ischemic model was made by occluding the anterior descending of the left artery (LAD) in rats. The change of ST segment and T wave of electrocardiograph (ECG) were observed, and the activity of lactate dehydrogenase (LDH), creatine kinase (CK), levels of the maleic dialdehyde (MDA), and nitric oxide (NO) in serum were measured. And by tetrazolium chloride (TTC) staining, the areas of myocardial infarction were observed. The expression of inducible nitricoxide synthase (iNOS) in rats was detected by emploring the reverse transcriptionpolymerase chain reaction (RT-PCR) technique. Results On the myocardial infarction model by occluding the anterior descending of the LAD in rats, TFRS (100 mg/kg) obviously reduced the height of ST segment after occluding 30 rain and TFRS (25, 50, and 100 mg/kg) obviously reduced the height of ST segment after reperfusion 30 min. TFRS (50 mg/kg) reduced by myocardial infarction area. TFRS (50 and 100 mg/kg) obviously reduced the activity of CK and LDH. TFRS (50 mg/kg) decreased the level of MDA in serum. By RT-PCR technique, it was found that the expression of iNOS mRNA in myocardium in IR rats pretreated with TFRS (100 mg/kg) was higher than that in IR and normal groups. Conclusions TFRS has the significant protection against myocardial ischemia-reperfusion injury via attenuating oxygen free radical and increasing the expression of iNOS mRNA and NO production.
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