Insulin alleviates mitochondrial oxidative stress involving upregulation of superoxide dismutase 2 and uncoupling protein 2 in septic acute kidney injury

Autor:	Ju‑Xing Zhang, Qi‑Yi Zeng, Guang‑Dao Chen, Jun‑Liang Zhang, Yi‑Ting Chen, Tao Wang
Jazyk:	angličtina
Rok vydání:	2018
Předmět:	0301 basic medicine Mitochondrial ROS Cancer Research medicine.medical_specialty insulin uncoupling protein 2 mitochondrial biogenesis medicine.medical_treatment SOD2 medicine.disease_cause Superoxide dismutase sepsis 03 medical and health sciences 0302 clinical medicine Immunology and Microbiology (miscellaneous) Internal medicine mitochondrial dysfunction medicine Uncoupling protein oxidative stress biology Chemistry Insulin 030208 emergency & critical care medicine General Medicine Articles Nitric oxide synthase 030104 developmental biology Endocrinology mitophagy Mitochondrial biogenesis acute kidney injury biology.protein Oxidative stress endogenous antioxidant system
Zdroj:	Experimental and Therapeutic Medicine
ISSN:	1792-1015 1792-0981
Popis:	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.
Databáze:	OpenAIRE
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