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(P<0.05);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(P<0.05);梗死区p ERK1/2蛋白表达水平明显高于非梗死区(P<0.05)。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(P>0.05)。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。
Objective To investigate the change of cardiac RAGE expression level in myocardial infarction rat model. Methods Myocardial infarction rat model was constructed by LAD ligation in Spraguee Dawley rats （230 ± 10）g. The mRNA level of RAGE in infarcted and non - infarcted regions of hearts was assessed by qPCR. The protein expression level was measured by immunohistochemistric and Western Blot analysis, and pERK1/2 levels were also detected by West- em Blot analysis. Results The RAGE mRNA level of infracted regions was significantly higher than that in non - infarc- ted regions （ P 〈 0. 05 ）. The protein expression of RAGE in infarcted regions was significantly increased comparing with that in non - infarcted regions （P 〈 0. 05 ）. The pERK1/2 expression level in infarcted regions was also significantly high- er than that in non - infarcted regions （ P 〈 0. 05 ）. There was no significant difference in RAGE mRNA level, RAGE pro- tein expression level or pERK1/2 expression level between cardiac tissue of Sham - operated group and non - infarcted re- gions of experimental group （ P 〉 0. 05 ）. Conclusion RAGE protein is activated in infarcted hearts tissues in rats, which increases the activation of MAPK/ERK1/2, subsequently leads to the activation of downstream cytokines, including NF - KB, finally induces overwhelming inflammatory and myocardial remodeling.
出处
《广东医学》
CAS
北大核心
2017年第10期1469-1472,共4页
Guangdong Medical Journal
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)
