线粒体ATP敏感性钾通道开放对大鼠肺缺血-再灌注损伤的保护作用Protective Effects of Opening of Mitochondrial ATP Sensitive Potassium Channel on Ischemia-reperfusion Injury in Rat Lung in vivo
李涛,赖春凤,曾茂森,陆德琴
LI Tao,LAI Chunfeng,ZENG Maosen,LU Deqin
摘要(Abstract):
目的:探讨线粒体ATP敏感性钾通道(mito KATP)开放对大鼠肺缺血-再灌注损伤(I/R)的保护作用。方法:建立大鼠肺I/R模型,设立假手术组、肺I/R组、mito KATP开放剂二氮嗪(DE)+I/R组、mito KATP阻断剂5-羟基葵酸(5-HD)+DE+I/R组,每组10只大鼠;检测各组肺组织湿/干重比,HE染色法观察各组肺组织形态学变化,免疫组织化学染色法检测肺组织细胞色素C的表达,TUNEL法检测肺细胞凋亡指数。结果:与假手术组相比,I/R组肺组织湿/干重比明显增加(P<0.05),肺组织出现出血、水肿等损伤性病理学变化,细胞色素C表达明显增多(P<0.01)、肺细胞凋亡指数明显增大(P<0.01);与I/R组相比,DE+I/R组肺组织湿/干重比明显降低(P<0.05)、肺组织损伤性病理变化明显减轻、肺细胞色素C表达明显减少(P<0.05)、细胞凋亡指数明显减小(P<0.05),而5-HD+DE+I/R组各项指标与I/R组比较无差异(P>0.05)。结论:mito KATP的开放可减轻肺水肿、抑制细胞凋亡,对大鼠肺缺血-再灌注损伤具有保护作用。
Objective: To investigate the protective effect of opening of mitochondrial ATP sensitive potassium channel on lung ischemia-reperfusion injury in rats. Methods: Pulmonary ischemia-reperfusion injury rat model was established by left hilar ligation and reperfusion. Preconditioning was conducted by using the mitochondrial ATP sensitive potassium channel opener( diazoxide,DE). Forty rats were randomly divided into four groups( n = 10,respectively),i. e. sham-operation group,I / R group,DE + I / R group and 5-HD + DE + I / R group. The ratio of wet / dry weight of lung tissue and morphological change were observed. Cytochrome C expression and apoptosis index in lung tissue were assessed by immunohistochemical staining and TUNEL methods,respectively. Results: Compared with sham-operation group,the wet / dry weight ratio of lung tissue in I / R group was significantly increased( P < 0. 05),the pathological changes such as hemorrhage and edema in lung tissue,the expression of cytochrome C increased significantly( P < 0. 01) and the lung cell apoptosis index increased significantly. Compared with I / R group,the wet / dry weight ratio of lung tissue in DE + I / R group was significantly decreased( P < 0. 05),the pathological changes in lung tissue were obviously alleviated,the expression of cytochrome C decreased significantly( P < 0. 01) and the lung cell apoptosis index decreased significantly( P < 0. 01). There was no difference in above-mentioned indexes between I / R group and 5-HD + I / R group( P > 0. 05). Conclusion: The opening of mitochondrial ATP sensitive potassium channel can effectively alleviate pulmonary edema,inhibit apoptosis and play a protective role in the injury of lung ischemia-reperfusion in vivo.
关键词(KeyWords):
肺;缺血;再灌注损伤;线粒体ATP敏感性钾通道;细胞凋亡;大鼠,Sprague-Dawley
lung;ischemia;reperfusion injury;mitochondrial ATP sensitive potassium channel;apoptosis;rats,Sprague-Dawley
基金项目(Foundation): 广东省梅州市科技局计划项目(2007B17)
作者(Author):
李涛,赖春凤,曾茂森,陆德琴
LI Tao,LAI Chunfeng,ZENG Maosen,LU Deqin
DOI: 10.19367/j.cnki.1000-2707.2015.04.008
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文章评论(Comment):
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- 肺
- 缺血
- 再灌注损伤
- 线粒体ATP敏感性钾通道
- 细胞凋亡
- 大鼠,Sprague-Dawley
lung - ischemia
- reperfusion injury
- mitochondrial ATP sensitive potassium channel
- apoptosis
- rats,Sprague-Dawley