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目的:观察芝麻素对大鼠心肌缺血-再灌注损伤的改善作用,并探讨其可能机制。方法:将50只大鼠随机分为正常对照组、假手术组、模型组及芝麻素高(160 mg/kg)、低(80 mg/kg)剂量组,每组10只,连续给药7 d。采用冠状动脉左前降支结扎40 min再灌注120 min的方法建立大鼠心肌缺血-再灌注损伤模型,比色法检测血清心肌肌钙蛋白Ⅰ(c TnⅠ)、乳酸脱氢酶(LDH)及血清和心肌组织总抗氧化能力(TAOC)、一氧化氮(NO)水平,并检测心肌组织Caspase-3活性;TUNEL染色法检测心肌细胞凋亡水平;Western blot法检测心肌组织内皮型一氧化氮合酶(eNOS)磷酸化水平、蛋白激酶B(Akt)蛋白磷酸化水平及超氧化物歧化酶(SOD)蛋白表达水平。结果:芝麻素预处理能明显改善缺血-再灌注所致大鼠心肌损伤,降低血清c TnⅠ、LDH水平,提高血清及心肌组织总抗氧化能力和NO水平(P<0.05或P<0.01),并能显著提高心肌组织SOD蛋白表达及Akt、eNOS蛋白磷酸化水平,降低Caspase-3活性,减少心肌细胞凋亡(P<0.05或P<0.01)。结论:芝麻素预处理能减轻缺血-再灌注所致大鼠心肌损伤,其机制与增强机体抗氧化能力、激活Akt/eNOS信号通路、增加NO合成,进而抑制心肌细胞凋亡有关。
Objective: To observe the effect of sesamin on myocardial ischemia-reperfusion injury in rats and to explore its possible mechanism. Methods: Fifty rats were randomly divided into normal control group, sham operation group, model group and sepsin high (160 mg / kg) and low (80 mg / kg) d. The model of myocardial ischemia-reperfusion injury was established by ligating the left anterior descending coronary artery for 40 min and reperfusion for 120 min. Serum cardiac troponin Ⅰ (cTnⅠ), lactate dehydrogenase (LDH) and The total antioxidant capacity (TAOC) and nitric oxide (NO) levels in serum, myocardium and myocardium were measured. Caspase-3 activity was detected by enzyme linked immunosorbent assay (ELISA). The apoptosis of cardiomyocytes was detected by TUNEL staining. (ENOS) phosphorylation, protein kinase B (Akt) phosphorylation and superoxide dismutase (SOD) protein expression. Results: Sesamin preconditioning could significantly improve the myocardial injury induced by ischemia-reperfusion, decrease the levels of cTnI and LDH, increase the total antioxidant capacity and NO level in serum and myocardium (P <0.05 or P <0.01) (P <0.05 or P <0.01), and significantly increased the expression of SOD and the phosphorylation of Akt and eNOS in myocardial tissue, decreased the activity of Caspase-3 and decreased the apoptosis of cardiomyocytes (P <0.05 or P <0.01). Conclusion: Sesamin preconditioning can attenuate myocardial injury induced by ischemia - reperfusion in rats. Its mechanism is related to enhancing the antioxidant capacity, activating Akt / eNOS signaling pathway, increasing NO synthesis, and then inhibiting cardiomyocyte apoptosis.