利拉鲁肽对大鼠心肌缺血再灌注损伤的作用研究

发布时间：2018-03-18 11:25

本文选题：心肌缺血再灌注损伤　切入点：心肌梗死面积　出处：《山西医科大学》2015年硕士论文　论文类型：学位论文

【摘要】：目的:研究利拉鲁肽对大鼠心肌缺血再灌注损伤的作用,进一步探讨其可能介导的机制。方法:SD大鼠48只,雄性,随机数字表法分为假手术组、缺血再灌注组(I/R组)和利拉鲁肽组。通过结扎左冠状动脉前降支(LAD)30 min再灌注2 h建立大鼠心肌缺血再灌注损伤的实验模型。苏木素伊红染色法光镜下观察大鼠心肌组织的病理形态学改变;2,3,5-三苯基氯化四氮唑染色法测定各组大鼠心肌梗死面积;免疫组织化学法测定心肌组织中半胱氨酸天冬氨酸蛋白酶-3(caspase-3)和P53的表达;黄嘌呤氧化酶法检测血清超氧化物歧化酶(SOD)活性,硫代巴比妥酸法测定丙二醛(MDA)浓度。结果:苏木素伊红染色结果示利拉鲁肽组大鼠心肌损伤程度明显较I/R组轻。与I/R组相比,利拉鲁肽组大鼠的心肌梗死面积较小[(0.44±0.08)%比(0.62±0.08)%,P0.05)],caspase-3表达水平较低(0.19±0.03比0.24±0.02,P0.05),p53的表达水平较低(0.27±0.03比0.39±0.04,P0.05),血清SOD活性较高(74.20±11.10比44.04±14.30,P0.05),MDA浓度较低(4.41±1.07比8.72±2.20,P0.05)。结论:利拉鲁肽可对抗大鼠心肌缺血再灌注损伤,对心肌具有保护作用,其机制可能由抗细胞凋亡和抗氧化应激作用介导。
[Abstract]:Objective: to study the effect of liralutide on myocardial ischemia-reperfusion injury in rats and to explore its possible mechanism. Methods: Forty-eight male SD rats were randomly divided into sham-operated group. Rat models of myocardial ischemia-reperfusion injury were established by ligating left anterior descending coronary artery (LADX) for 30 min and reperfusion for 2 hours. The rat heart was observed with hematoxylin and eosin red staining under light microscope. The histopathological changes of muscle tissue of rats were determined by staining method of 5-triphenyl tetrazolium chloride (5-triphenyl tetrazolium chloride). The expression of caspase-3 and p53 in myocardial tissue was determined by immunohistochemical method, and the activity of serum superoxide dismutase (SOD) was detected by xanthine oxidase method. Results: the results of hematoxylin eosin staining showed that the degree of myocardial injury in the group of liraropeptide was significantly less than that in the group I / R, and compared with that in the group I / R, and compared with that in the group I / R, the concentration of MDAs was determined by thiobarbituric acid method. The expression level of caspase-3 was lower in the group of Lilalutide (0.44 卤0.08% vs 0.62 卤0.08% vs 0.62 卤0.08% than 0.62 卤0.08). The expression level of caspase-3 was 0.19 卤0.03 vs 0.24 卤0.02P0.05P0.05.The expression of p53 was lower than 0.27 卤0.03 vs 0.39 卤0.04P0.05A, and the activity of serum SOD was 74.20 卤11.10 vs 44.04 卤14.30P0.05 respectively. It may be mediated by anti-apoptosis and anti-oxidative stress.
【学位授予单位】：山西医科大学
【学位级别】：硕士
【学位授予年份】：2015
【分类号】：R542.2

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