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目的:研究氧化苦参碱(oxymatrine,OMT)对大鼠冠脉结扎诱发急性实验性心肌梗死的作用及可能作用机制。方法:SD大鼠按体重随机分为4组:假手术组、模型组、OMT 50,25 mg.kg-1组,各组ig给药,连续5 d。末次给药后1 h结扎冠状动脉左前降支(LAD)复制大鼠急性实验性心肌梗死模型,6 h后,收集分析标本。HE染色观察大鼠心肌组织病理形态学变化,生化分析法检测血清中过氧化氢酶(CAT)、超氧化物岐化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)的活力,总抗氧化能力(T-AOC)及丙二醛(MDA)含量,ELISA法分析血清中白介素-1β(IL-1β)、白介素-6(IL-6)、和肿瘤坏死因子-α(TNF-α)的水平。结果:OMT 50 mg.kg-1组能明显改善急性心肌梗死所致心肌组织间质水肿、炎细胞浸润等病理组织学改变;提高心肌梗死大鼠血清中SOD,CAT,GHS-Px活性,降低大鼠血清中MDA含量(与模型组比较,P<0.05或P<0.01);降低心肌梗死大鼠血清中IL-1β,IL-6,TNF-α的水平(P<0.05或P<0.01);对血清中T-AOC未见明显影响。结论:OMT对大鼠冠状动脉结扎诱发实验性急性心肌梗死具有一定的保护作用,其作用机制可能与抑制免疫炎症因子分泌和改善氧化应激状态有关。
Objective: To investigate the effect of oxymatrine (OMT) on acute experimental myocardial infarction induced by coronary artery ligation in rats and its possible mechanism. Methods: SD rats were randomly divided into 4 groups according to body weight: sham-operation group, model group, OMT 50, 25 mg.kg-1 group. Each group was administered with ig for 5 consecutive days. Rats were sacrificed at 1 h after the last administration of LAD to establish acute experimental myocardial infarction model. Six hours later, the specimens were collected and analyzed. The pathological changes of myocardial tissue were observed by HE staining. The contents of catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) (T-AOC) and malondialdehyde (MDA) were detected by enzyme linked immunosorbent assay (ELISA). The levels of interleukin-1β, interleukin-6 and tumor necrosis factor- TNF-α) levels. Results: OMT 50 mg.kg-1 group could significantly improve the histopathological changes of myocardial interstitial edema and inflammatory cell infiltration induced by acute myocardial infarction, and increase the activities of SOD, CAT and GHS-Px in the serum of myocardial infarction rats The level of IL-1β, IL-6 and TNF-α in the serum of rats with myocardial infarction (P <0.05 or P <0.01) ; No significant effect on T-AOC in serum. CONCLUSION: OMT has a protective effect on experimental acute myocardial infarction induced by coronary artery ligation in rats, and its mechanism may be related to inhibiting the secretion of inflammatory cytokines and improving the oxidative stress status.