急性心肌梗死时晚期糖基化终末产物受体表达水平的改变

发布时间：2018-03-09 12:29

本文选题：晚期糖基化终产物受体　切入点：心肌梗死　出处：《广东医学》2017年10期 　论文类型：期刊论文

【摘要】：目的研究大鼠急性心肌梗死时心脏晚期糖基化终产物受体(RAGE)表达水平的改变。方法将体重(230±20)g的SD大鼠随机分为实验组和假手术组,两组均在麻醉下打开胸腔挤出心脏,实验组用6号手术线在左心耳下1.5~2 mm处结扎冠状动脉左前降支建立急性心肌梗死模型,假手术组不结扎,之后将心脏放回胸腔,关闭切口;3周后处死大鼠,取心脏不同部位心肌组织,应用定量PCR技术检测RAGE基因mRNA表达水平;应用免疫组织化学和Western blot方法检测RAGE蛋白表达水平;应用Western blot方法检测ERK1/2蛋白表达水平。结果实验组梗死区心肌组织RAGE的mRNA水平较非梗死区明显升高(P0.05);免疫组织化学及Western blot分析显示梗死区RAGE蛋白表达水平明显较非梗死区高(P0.05);梗死区p ERK1/2蛋白表达水平明显高于非梗死区(P0.05)。假手术组心肌组织RAGE的mRNA和蛋白表达水平、p ERK1/2蛋白表达水平与实验组非梗死区心肌组织比较差异无统计学意义(P0.05)。结论大鼠心肌梗死后,梗死区心肌组织RAGE被激活,并通过MAPK/ERK1/2途径进一步激活核因子-κB等下游信号转导因子,最终引起一系列促炎反应并导致心肌重构。
[Abstract]:Objective to study the acute myocardial infarction rat cardiac receptor for advanced glycation end products (RAGE). Methods the changes of expression level of body weight (230 + 20) g SD rats were randomly divided into experimental group and sham operation group, the two groups were under anesthesia and open the chest extrusion heart, the experimental group with 6 Gillespie operation the line in the left atrium 1.5~2 mm left anterior descending coronary artery was ligated to establish acute myocardial infarction model, ligation, the heart back into the chest, close the incision; after 3 weeks the rats were sacrificed and hearts from different parts of myocardial tissue, RAGE gene was detected by quantitative mRNA PCR expression; immune histochemical and Western blot method to detect the expression level of RAGE protein; application of Western blot methods to detect the expression level of ERK1/2 protein. Results the myocardial tissue in experimental group RAGE mRNA levels were significantly higher in non infarct zone (P0.05); free chemical and Wester epizootics N blot analysis showed that the expression level of RAGE protein was significantly higher than non infarcted area of infarction area (P0.05); the expression of P in infarction area ERK1/2 protein level was significantly higher than that in non infarct zone (P0.05). The expression of mRNA and protein in sham operation group, myocardial RAGE, P protein expression level of ERK1/2 in the experimental group and the non infarcted myocardium area difference no statistical significance (P0.05). Conclusion myocardial infarction rats after myocardial infarction RAGE is activated, and MAPK/ERK1/2 by the way of further activation of nuclear factor kappa B downstream signal transduction factor, resulting in a series of inflammatory responses and cause myocardial remodeling.

【作者单位】：南方医科大学;广东省人民医院(广东省医学科学院)广东省心血管病研究所心内科;
【基金】：广东省自然科学基金资助项目(编号:2016A030313796) 广州市科技计划科学研究专项项目(编号:201510010190)
【分类号】：R542.22

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