Alaabta

Si loo baaro doorka cadaadiska oksaydhiyaha iyo / ama naafanimada mitochondrial ee dhacdada dhaawaca kelyaha ee degdega ah (AKI) inta lagu jiro sepsis, waxaan samaynay sepsis-ku-abuuray qaabka vitro iyadoo la adeegsanayo unugyo epithelial ah oo u dhow oo soo gaadhay endotoxin bakteeriyada (lipopolysaccharide, LPS).Baadhitaankani wuxuu bixiyay sifooyin muhiim ah oo ku saabsan xidhiidhka ka dhexeeya cadaadiska oksaydhiyaha iyo cilladaha dhaqdhaqaaqa silsiladaha neefsiga ee mitochondrial.Daaweynta LPS waxay keentay kororka muujinta nitric oxide synthase (iNOS) iyo NADPH oxidase 4 (NOX-4), taasoo soo jeedinaysa muujinta xad-dhaafka ah ee cytosolic ee nitric oxide iyo anion superoxide, noocyada nitrogen ee asaasiga ah (RNS) iyo noocyada oksijiinta firfircoon. (ROS).Xaaladdan oksaydhiyuhu waxay u muuqatay inay joojisay fosforyaalka oksaydhka mitochondrial iyadoo hoos u dhigaysa dhaqdhaqaaqa cytochrome c oxidase.Natiijo ahaan, khalkhal ku yimid gaadiidka elektaroonigga ah iyo bamgareynta proton-ka guud ahaan xuubka gudaha ee mitochondrial ayaa dhacay, taasoo keentay hoos u dhaca awoodda xuubka mitochond, sii-deynta arrimo keena apoptotic-ka iyo hoos u dhaca adenosine triphosphate.Waxa xiiso leh, ka dib markii ay bartilmaameedsadeen RNS iyo ROS, mitochondria waxay noqotay soo saaraha ROS, taas oo ka qayb qaadatay kordhinta cilladda mitochondrial.Doorka oksaydhiyeyaasha ee cillad la'aanta mitochondrial waxaa sii xaqiijiyay isticmaalka iNOS inhibitors ama antioxidants kuwaas oo ilaaliya dhaqdhaqaaqa cytochrome c oxidase kana hortagaya xuubabka mitochondrial ee suurtogalka ah.Natiijooyinkani waxay soo jeedinayaan in sepsis-ku-soo-baxa AKI aan loo tixgalin oo kaliya inuu yahay fashilka heerka tamarta laakiin sidoo kale jawaab celin isku dhafan, oo ay ku jiraan dhacdooyinka qoraalka, calaamadaynta ROS, dhaqdhaqaaqa mitochondrial iyo jihada dheef-shiid kiimikaadka sida apoptosis.