自噬在急性心肌梗死后無復(fù)流中的表達(dá)
發(fā)布時間：2018-08-30 12:10
【摘要】：目的觀察急性心肌梗死后無復(fù)流區(qū)心肌細(xì)胞自噬的表達(dá),探討心肌細(xì)胞自噬在大鼠實驗性無復(fù)流中的作用。方法 SD大鼠隨機分為實驗組和對照組:均予結(jié)扎冠狀動脈2 h,再灌注1 h,建立急性心肌梗死后再灌注無復(fù)流模型,對照組只穿線,不結(jié)扎。在再灌注末,從左心房注入6%硫磺素1 m L/kg使復(fù)流區(qū)著色,無復(fù)流區(qū)不著色;再于原位重新結(jié)扎冠狀動脈,實驗組從左心房注入Evan'S藍(lán),使結(jié)扎區(qū)外著藍(lán)色,梗死區(qū)不著藍(lán)色,對照組不予Evan's藍(lán)。采用實時定量PCR法和Western blot法檢測實驗組無復(fù)流區(qū)、梗死區(qū)和正常區(qū)心肌組織自噬相關(guān)蛋白LC3、p62/SQSTM1表達(dá);電鏡下觀察自噬體超微結(jié)構(gòu)改變情況。結(jié)果 TTC和硫磺素染色結(jié)果顯示,實驗組無復(fù)流面積顯著高于對照組(P0.05);透射電鏡觀察到,大鼠心肌細(xì)胞內(nèi)自噬體體積增大,數(shù)量增多;PCR法和Western blot法檢測實驗組無復(fù)流區(qū)、梗死區(qū)及正常區(qū)心肌組織自噬相關(guān)蛋白LC3-Ⅰ、LC3-Ⅱ,p62/SQSTM1的表達(dá),實驗組無復(fù)流區(qū)自噬表達(dá)明顯高于梗死區(qū)和正常區(qū)心肌組織(P0.05),但梗死區(qū)和遠(yuǎn)端區(qū)心肌組織自噬表達(dá)差異無統(tǒng)計學(xué)意義(P0.05)。結(jié)論實驗組無復(fù)流區(qū)心肌組織局部自噬表達(dá)增強,其活性的改變可能與無復(fù)流的發(fā)展及程度相關(guān)。
[Abstract]:Objective to observe the expression of myocardial autophagy in non-reflow zone after acute myocardial infarction (AMI) and to investigate the role of myocardial autophagy in experimental non-reflow rats. Methods SD rats were randomly divided into experimental group and control group: coronary artery was ligated for 2 hours and reperfusion for 1 hour. At the end of reperfusion, the reflow area was stained by injecting 6% sulfur 1 m L/kg from the left atrium, and the no reflow area was not stained, and then the coronary artery was religated in situ, and the Evan'S blue was injected into the left atrium in the experimental group, so that the ligation area was blue outside the ligation area and the infarcted area was not blue. The control group was not treated with Evan's blue. Real time quantitative PCR and Western blot were used to detect the expression of autophagy associated protein (LC3,p62/SQSTM1) in myocardium without reflow, infarction and normal myocardium, and ultrastructural changes of autophagy were observed under electron microscope. Results the results of TTC and sulfur staining showed that the no reflow area in the experimental group was significantly higher than that in the control group (P0.05). Expression of autophagy associated protein LC3- 鈪，
本文編號：2213033
[Abstract]:Objective to observe the expression of myocardial autophagy in non-reflow zone after acute myocardial infarction (AMI) and to investigate the role of myocardial autophagy in experimental non-reflow rats. Methods SD rats were randomly divided into experimental group and control group: coronary artery was ligated for 2 hours and reperfusion for 1 hour. At the end of reperfusion, the reflow area was stained by injecting 6% sulfur 1 m L/kg from the left atrium, and the no reflow area was not stained, and then the coronary artery was religated in situ, and the Evan'S blue was injected into the left atrium in the experimental group, so that the ligation area was blue outside the ligation area and the infarcted area was not blue. The control group was not treated with Evan's blue. Real time quantitative PCR and Western blot were used to detect the expression of autophagy associated protein (LC3,p62/SQSTM1) in myocardium without reflow, infarction and normal myocardium, and ultrastructural changes of autophagy were observed under electron microscope. Results the results of TTC and sulfur staining showed that the no reflow area in the experimental group was significantly higher than that in the control group (P0.05). Expression of autophagy associated protein LC3- 鈪，
本文編號：2213033
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