CAJ | 학술논문

目的：评价线粒体融合?分裂在大鼠内毒素性急性肺损伤中的作用。方法健康雄性SD大鼠20只，体重160～180 g，2月龄，采用随机数字表法，将其分为2组（ n＝10）：正常对照组（ C组）及内毒素性急性肺损伤组（L组）。 L组静脉注射LPS 5 mg∕kg，C组给予等容量生理盐水0．5 ml，给予LPS后6 h时处死大鼠，取肺组织，测定湿重∕干重（ W∕D）比值、超氧化物歧化酶（ SOD）活性和丙二醛（ MDA）含量；测定线粒体融合相关蛋白[线粒体融合蛋白1（ Mfn1）、线粒体融合蛋白2（ Mfn2）和视神经萎缩蛋白1（OPA1）]及其 mRNA 的表达，并测定线粒体分裂相关蛋白[动力相关蛋白1（ Drp1）和分裂蛋白1（ Fis1）]及其mRNA的表达。结果与C组比较，L组肺组织W∕D比值和MDA含量升高，肺组织SOD活性降低；肺组织Mfn1、Mfn2和OPA1及其mRNA的表达下调，肺组织Drp1和Fis1及其mRNA的表达上调（ P＜0．05）。 L组肺组织病理学损伤明显重于C组。结论大鼠内毒素性急性肺损伤的机制与线粒体融合减少、分裂增多导致氧化应激反应增强有关。
목적：평개선립체융합?분렬재대서내독소성급성폐손상중적작용。방법건강웅성SD대서20지，체중160～180 g，2월령，채용수궤수자표법，장기분위2조（ n＝10）：정상대조조（ C조）급내독소성급성폐손상조（L조）。 L조정맥주사LPS 5 mg∕kg，C조급여등용량생리염수0．5 ml，급여LPS후6 h시처사대서，취폐조직，측정습중∕간중（ W∕D）비치、초양화물기화매（ SOD）활성화병이철（ MDA）함량；측정선립체융합상관단백[선립체융합단백1（ Mfn1）、선립체융합단백2（ Mfn2）화시신경위축단백1（OPA1）]급기 mRNA 적표체，병측정선립체분렬상관단백[동력상관단백1（ Drp1）화분렬단백1（ Fis1）]급기mRNA적표체。결과여C조비교，L조폐조직W∕D비치화MDA함량승고，폐조직SOD활성강저；폐조직Mfn1、Mfn2화OPA1급기mRNA적표체하조，폐조직Drp1화Fis1급기mRNA적표체상조（ P＜0．05）。 L조폐조직병이학손상명현중우C조。결론대서내독소성급성폐손상적궤제여선립체융합감소、분렬증다도치양화응격반응증강유관。
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.