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Insulin alleviates mitochondrial oxidative stress involving upregulation of superoxide dismutase 2 and uncoupling protein 2 in septic acute kidney injury.
Chen, Guang-Dao; Zhang, Jun-Liang; Chen, Yi-Ting; Zhang, Ju-Xing; Wang, Tao; Zeng, Qi-Yi.
Afiliación
  • Chen GD; Center of Pediatrics, Zhujiang Hospital, Southern Medical University, Guangzhou, Guangdong 510280, P.R. China.
  • Zhang JL; Department of Pediatrics, Central Hospital of Panyu District, Guangzhou, Guangdong 511400, P.R. China.
  • Chen YT; Center of Pediatrics, Zhujiang Hospital, Southern Medical University, Guangzhou, Guangdong 510280, P.R. China.
  • Zhang JX; Department of Neonatology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong 510515, P.R. China.
  • Wang T; Center of Pediatrics, Zhujiang Hospital, Southern Medical University, Guangzhou, Guangdong 510280, P.R. China.
  • Zeng QY; Center of Pediatrics, Zhujiang Hospital, Southern Medical University, Guangzhou, Guangdong 510280, P.R. China.
Exp Ther Med ; 15(4): 3967-3975, 2018 Apr.
Article en En | MEDLINE | ID: mdl-29563990
The aim of the present study was to explore the effects and mechanisms of insulin on mitochondrial oxidative stress in septic acute kidney injury (AKI). Male Sprague Dawley rats were divided randomly into four groups: Control group, sham surgery group, cecal ligation and puncture (CLP) group, and CLP plus insulin group. Blood specimens and kidney tissues were obtained at 12 and 24 h after surgery as separate experiments. Analyses of histology and indicators of renal injury [blood urea nitrogen (BUN) and serum creatinine (CRE) and neutrophil gelatinase-associated lipocalin (NGAL)], mitochondrial function [adenosine triphosphate (ATP) and mitochondrial membrane potential (MMP)], oxidative stress [inducible nitric oxide synthase (iNOS), reactive oxygen species (ROS) and nitric oxide (NO)], endogenous antioxidant systems [superoxide dismutase (SOD) and glutathione (GSH)] as well as the expression of uncoupling protein (UCP), PINK1 protein (a major mediator of mitophagy), PGC1α protein (a major regulator of mitochondrial biogenesis) were performed. Compared with CLP group, the CLP plus insulin group had milder histological damage, higher levels of ATP and MMP as well as lower levels of BUN, serum CRE and NGAL, intrarenal iNOS, mitochondrial ROS and total NO. Moreover, the CLP plus insulin group demonstrated increased expression of SOD2 and UCP2. In contrast, insulin administration suppressed mitophagy meanwhile did not upregulate total GSH and induce mitochondrial biogenesis following CLP. These findings indicated that the upregulation of SOD2 and UCP2 may be involved in insulin protecting against mitochondrial oxidative stress in septic AKI.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Idioma: En Revista: Exp Ther Med Año: 2018 Tipo del documento: Article Pais de publicación: Grecia
Texto completo
Añadir a Mi BVS
Imprimir
XML
PubMed Links
Buscar en Google

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Idioma: En Revista: Exp Ther Med Año: 2018 Tipo del documento: Article Pais de publicación: Grecia