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机构地区:[1]长治医学院附属和济医院心内科,山西长治046000
出 处:《中国医药指南》2016年第11期5-5,7,共2页Guide of China Medicine
基 金:长治市科技局课题(20123059)
摘 要:目的建立缺血再灌注模型,观察阿托伐他汀、尼可地尔后处理对兔心肌缺血再灌注损伤的保护作用,并对其作用机制进行研究。方法 50只大白兔随机分成5组A^E(空白对照组A组、平行对照组B组、阿托伐他汀组C组、尼可地尔组D组、联合后处理组E组),采用"二线二结法"建立缺血再灌注模型。各组按照实验设计方案给药。试剂盒检测SOD、MDA。电镜检测心肌超微结构的变化。RT-PCR检测HIF-1α。结果 1与A组相比,B^E组血清MDA含量明显增加(P<0.05),而SOD明显降低(P<0.01);与B组比较,C^E组血清MDA含量显著降低(P<0.01),SOD活性显著提高(P<0.01);与C、D组比较,E组MDA含量及SOD活性均无显著性差异(P>0.05)。2电镜观察,缺血后处理组心肌细胞的损伤明显减轻。3 RT-PCR检测HIF-1α,与A组相比,B^E组HIF-1αm RNA表达增高(P<0.01),显示缺血再灌注能增强其表达;其中C^E组又较B组增高(P<0.05),显示缺血后处理更能增强其表达。结论 1阿托伐他汀、尼可地尔后处理对兔心肌缺血再灌注损伤有保护作用,可以改善再灌注后心肌的组织结构。2阿托伐他汀、尼可地尔后处理可能通过减轻氧化应激、减轻细胞凋亡发挥心肌保护作用。Objective To observe the cardio protective effect of myocardial ischemic postconditioning against ischemia and reperfusion induced injury in rabbit heart. Methods 50 rabbits were randomly divided into 5 groups, and the myocardial ischemia-reperfusion were generated by two sutures and two knots, and then administrated in accordance with the experimental design, testing SOD and MDA in serum, observing the changes of myocardial structure, testing HIF-1α by RT-PCR. Results The MDA levels of group C-E were significantly lower than B(P〈0.01) but the SOD were higher than B(P〈0.01). The injury of group B was worse than C-E of the cellular structure under EM. The HIF-1αm RNA levels of group B-E were higher than that of group A(P〈0.01), and C-E higher than B(P〈0.05). Conclusion Myocardial isehemic postconditioning of atorvastatin and nicorandil induced cardio protection against ischemia reperfusion injury in rabbits. They can improve structure under microscope, maybe through reducing oxidative stress and reducing cell apoptosis.
分 类 号:R54[医药卫生—心血管疾病]
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