Role of mitochondrial fusion-fission in endotoxin-induced acute lung injury in rats
10.3760/cma.j.issn.0254.1416.2015.05.023
- VernacularTitle:线粒体融合-分裂在大鼠内毒素性急性肺损伤中的作用
- Author:
Ying WANG
;
Dan WANG
;
Jianbo YU
;
Lirong GONG
;
Yuan ZHANG
;
Shuan DONG
;
Rui MU
;
Jia SHI
;
Daquan LIU
- Publication Type:Journal Article
- Keywords:
Mitochondrial proteins;
Respiratory distress syndrome,adult;
Endotoxemia;
Mi-tochondrial fusion;
Mitochondrial fission
- From:
Chinese Journal of Anesthesiology
2015;(5):604-607
- CountryChina
- Language:Chinese
-
Abstract:
Objective To evaluate the role of mitochondrial fusion?fission in endotoxin?induced a?cute lung injury in rats. Methods Twenty healthy male Sprague?Dawley rats, weighing 160-180 g, were e?qually and randomly divided into either control group ( group C ) or endotoxin?induced acute lung injury group (group L) using a random number table. Lipopolysaccharide 5 mg∕kg was injected intravenously in group L, while the equal volume of normal saline 0?5 ml was given instead in group C. The animals were sacrificed at 6 h after administration of lipopolysaccharide or normal saline. The lungs were immediately re?moved for measurement of wet to dry lung weight ratio ( W∕D ratio) , superoxide dismutase ( SOD) activity and malondialdehyde ( MDA) content. The mitochondrial fusion proteins mitofusin 1 ( Mfn1) , Mfn2 and op?tic atrophy 1 ( OPA1) mRNA and protein expression was detected, and mitochondrial fission proteins dy?namin?related protein 1 (Drp1) and fission 1 (Fis1) mRNA and protein expression was also detected in lung tissues. Results Compared to group C, the W∕D ratio and MDA contents in lung tissues were signifi?cantly increased, SOD activity was decreased, Mfn1, Mfn2 and OPA1 mRNA and protein expression in lung tissues was down?regulated, and Drp1 and Fis1 mRNA and protein expression was up?regulated in group L. The pathological damage to lung tissues was obviously aggravated in group L when compared to group C. Conclusion The mechanism underlying endotoxin?induced acute lung injury is related to enhanced oxidative stress responses caused by decreased mitochondrial fusion and increased mitochondrial fission in rats.
