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机构地区:[1]南京医科大学附属无锡市人民医院麻醉科,214023
出 处:《中华麻醉学杂志》2015年第4期426-429,共4页Chinese Journal of Anesthesiology
摘 要:目的 评价内质网应激在大鼠肺缺血再灌注损伤中的作用.方法 健康成年雄性SD大鼠56只,体重250~320 g,采用随机数字表法分为2组:假手术组(S组,n=16)和肺缺血再灌注组(I/R组,n=40).采用阻断左肺门60 min再灌注的方法建立大鼠原位肺缺血再灌注损伤模型.于缺血前、再灌注即刻、1、2和4h时取动脉血样,测定PaO2和PaCO2;处死大鼠,取肺组织,观察病理学结果,计算湿重/干重(W/D)比值,分别采用Western blot法和RT-PCR法测定内质网分子伴侣葡萄糖调节蛋白78(GRP78)和C/EBP同源蛋白(CHOP)蛋白及其mRNA的表达水平.结果 与S组比较,I/R组再灌注期间PaO2降低,PaCO2升高,W/D比值升高,肺组织GRP78和CHOP蛋白及其mRNA表达上调(P<0.01),肺组织发生病理学损伤.随再灌注时间延长,I/R组肺损伤逐渐加重,同时肺组织GRP78和CHOP蛋白及其mRNA表达逐渐上调(P<0.05).结论 过度的内质网应激可能是大鼠肺缺血再灌损伤的病理生理机制之一.Objective To investigate the role of endoplasmic reticulum stress in lung ischemiareperfusion (I/R) injury in rats.Methods Fifty-six healthy male Sprague-Dawley rats,weighing 250-320 g,were randomly divided into 2 groups using a random number table:sham operation group (group S,n=16) and I/R group (n=40).Lung I/R was induced by clamping the left hilum of lung for 60 min followed by reperfusion.Before ischemia (T0) and at 0,1,2 and 4 h (T4) of reperfusion,PaO2 and PaCO2 were recorded.The rats were sacrificed,and lungs were removed for examination of pathological changes.Wet/dry lung weight ratio (W/D ratio) was calculated.The expression of molecular chaperones of 78-kDa glucose-regulated protein (GRP78) and C/EBP homologous protein (CHOP) protein and mRNA was detected in lung tissues using Western blot and real-time PCR,respectively.Results Compared with group S,PaO2was significantly decreased,PaCO2 and W/D ratio were increased,and the expression of GRP78 and CHOP protein and mRNA was up-regulated during reperfusion,and the pathological changes of lungs were found in group I/R.With the prolongation of reperfusion,the pathological changes of lungs were gradually aggravated,and the expression of GRP78 and CHOP protein and mRNA was gradually up-regulated in group I/R.Conclusion Excessive endoplasmic reticulum stress may be one of the pathophysiological mechanisms of lung I/R injury in rats.
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