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目的:研究薯蓣皂苷药理性预适应对大鼠心肌缺血/再灌注损伤的保护作用,并从氧化-抗氧化角度初步探讨其作用机制。方法:大鼠被随机分为缺血/再灌注(I/R)、心脏缺血预适应(CIP)、薯蓣皂苷高剂量(DH)、薯蓣皂苷低剂量(DL)4组。I/R、CIP组0.9%生理盐水10 ml/kg灌胃,DH、DL组薯蓣皂苷279mg/kg、139.5mg/kg灌胃,连续7d。末次给药24 h后,各组动物均经历心肌缺血/再灌注损伤,CIP组于缺血前行心肌缺血预适应。连续监测血压和心电图变化,检测心肌梗死范围,测定血浆中肌酸激酶(CK)活性及NO含量,检测心肌组织中超氧化物歧化酶(SOD)活性、丙二醛(MDA)含量,RT-PCR检测心肌组织Mn-SOD表达。结果:与I/R组相比,CIP、DH及DL组ST-段抬高幅度降低,室早和室速出现时间推迟,持续时间缩短,心肌梗死范围缩小,NO、SOD活性升高,Mn-SOD表达增强,CK活力下降,MDA含量减少。结论:薯蓣皂苷对具有与CIP程度相当的心脏保护作用,其机制与增强心肌抗氧化能力有关。
Objective: To study the protective effect of pharmacological preconditioning of diosgenin on myocardial ischemia/reperfusion injury in rats, and to explore its mechanism of action from the perspective of oxidation-antioxidation. METHODS: Rats were randomly divided into 4 groups: ischemia/reperfusion (I/R), cardiac ischemic preconditioning (CIP), high dose of dioscin (DH), and low dose of dioscin (DL). I / R, CIP group 0.9% saline 10 ml / kg gavage, DH, DL group dioscin 279mg/kg, 139.5mg/kg gavage, continuous 7d. After 24 h of the last administration, all groups of animals underwent myocardial ischemia/reperfusion injury. In the CIP group, myocardial ischemic preconditioning was performed before ischemia. Continuous monitoring of blood pressure and electrocardiogram changes, detection of myocardial infarct size, determination of plasma creatine kinase (CK) activity and NO content, detection of myocardial superoxide dismutase (SOD) activity, malondialdehyde (MDA) content, RT-PCR Detect myocardial tissue Mn-SOD expression. Results: Compared with I/R group, ST-segment elevation decreased in CIP, DH, and DL groups. Delayed ventricular tachycardia and delayed ventricular tachycardia, shortened duration, reduced myocardial infarct size, increased NO and SOD activity, Mn- SOD expression increased, CK activity decreased, and MDA content decreased. CONCLUSION: Dioscin has a cardioprotective effect comparable to that of CIP, and its mechanism is related to the enhancement of myocardial antioxidation ability.