观察淫羊藿总黄酮(total flavones of Epimedium,TFE)对大鼠心肌急性缺血再灌注损伤氧化应激干预作用及其机制。40只雄性大鼠随机分为假手术组,模型组,地尔硫卓组(阳性对照药)以及淫羊藿总黄酮高、低剂量组,每组8只。淫羊藿总黄酮分别以200,100 mg·kg~(-1)的剂量连续灌胃给药4 d后,结扎冠状动脉前降支40 min再灌注4 h建立大鼠急性心肌缺血再灌注损伤模型。采用N-BT染色法测定心肌梗死范围,比色法检测心肌组织中SOD和T-AOC活性及MDA含量,ELISA法测定血清Tn I水平,同时光镜下观察心肌组织结构的变化,分别应用免疫组化和Western blot法观察心肌组织中SIRT1与Nrf2表达的变化。结果发现,与模型组比较,淫羊藿总黄酮高、低剂量组以及地尔硫卓组能明显减少心肌梗死范围,降低血清Tn I水平,提高心肌组织中SOD和T-AOC活性并降低MDA含量(P<0.05或P<0.01),改善缺血再灌注损伤后心肌的组织结构,同时淫羊藿总黄酮高、低剂量组中心肌组织SIRT1和Nrf2表达明显增加(P<0.05或P<0.01)。由此可见,淫羊藿总黄酮能够通过提高机体SIRT1与Nrf2内源性抗氧化信号传导通路,增加心肌组织的抗过氧化能力,从而抑制心肌急性缺血再灌注过程中氧化应激反应导致的心肌细胞不可逆性伤害,维护心肌组织的正常功能。 To observe the effect of total flavones of Epimedium (TFE) on oxidative stress induced by acute myocardial ischemia / reperfusion in rats and its mechanism. Forty male rats were randomly divided into sham operation group, model group, diltiazem group (positive control drug) and epimedium high and low dose group, 8 rats in each group. Herba Epimedii flavonoids were administrated orally for 200 d at doses of 200 and 100 mg · kg ~ (-1) respectively for 4 d, ligated the anterior descending coronary artery for 40 min and reperfused for 4 h to establish acute myocardial ischemia-reperfusion injury model . The extent of myocardial infarction was determined by N-BT staining. The activity of SOD and T-AOC and the content of MDA were detected by colorimetry. The level of serum TnI was measured by ELISA. The changes of myocardial tissue were observed under light microscope. The changes of SIRT1 and Nrf2 in myocardium were observed by immunohistochemistry and Western blot. The results showed that compared with the model group, epimedium total flavonoids high, low dose group and diltiazem group can significantly reduce the range of myocardial infarction, reduce serum Tn I levels, increase myocardial SOD and T-AOC activity and reduce the content of MDA (P <0.05 or P <0.01). The myocardial structure was also improved after ischemia-reperfusion injury. The expression of SIRT1 and Nrf2 in myocardial tissue of high and low dose epimedium flavonoids groups increased significantly (P <0.05 or P <0.01). Thus, the total flavonoids of Epimedium can enhance the anti-peroxidation ability of myocardial tissue by increasing the endogenous antioxidant signaling pathways of SIRT1 and Nrf2 in the body and thereby inhibit the oxidative stress response during acute myocardial ischemia / reperfusion Cardiomyocyte irreversible damage, maintaining the normal function of myocardial tissue.