Kayayyaki

Don bincika rawar da damuwa na oxidative da / ko mitochondrial nakasar a cikin abin da ya faru na m koda rauni (AKI) a lokacin sepsis, mun samar da wani sepsis-induced in vitro model ta yin amfani da proximal tubular epithelial Kwayoyin fallasa zuwa wani kwayan cuta endotoxin (lipopolysaccharide, LPS).Wannan binciken ya ba da mahimman fasalulluka akan alakar da ke tsakanin damuwa mai iskar oxygen da lahani na sarkar numfashi na mitochondrial.Jiyya na LPS ya haifar da karuwa a cikin maganganun inducible nitric oxide synthase (iNOS) da NADPH oxidase 4 (NOX-4), yana ba da shawarar cytosolic overexpression na nitric oxide da superoxide anion, nau'in nitrogen mai amsawa na farko (RNS) da nau'in oxygen mai aiki. (ROS).Wannan yanayin oxidant kamar yana katse mitochondrial oxidative phosphorylation ta hanyar rage ayyukan cytochrome c oxidase.A sakamakon haka, rushewar jigilar lantarki da kuma famfo proton a cikin membrane na ciki na mitochondrial ya faru, wanda ke haifar da raguwar yuwuwar yuwuwar mitochond rial, sakin abubuwan da ke haifar da apoptotic da raguwar adenosine triphosphate.Abin sha'awa, bayan da RNS da ROS suka yi niyya, mitochondria ya zama mai samar da ROS, don haka yana ba da gudummawar haɓaka tabarbarewar mitochondrial.Matsayin oxidants a cikin tabarbarewar mitochondrial an ƙara tabbatar da shi ta hanyar amfani da masu hana iNOS ko antioxidants waɗanda ke adana ayyukan cytochrome c oxidase kuma suna hana yiwuwar ɓarnawar mitochondrial membrane.Wadannan sakamakon sun ba da shawarar cewa AKI da ke haifar da sepsis ba wai kawai za a yi la'akari da gazawar matsayin makamashi ba amma har ma a matsayin amsawar haɗin kai, ciki har da abubuwan da suka faru na rubuce-rubuce, siginar ROS, aikin mitochondrial da daidaitawar rayuwa kamar apoptosis.