Open Access

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

  • Authors:
    • Guang‑Dao Chen
    • Jun‑Liang Zhang
    • Yi‑Ting Chen
    • Ju‑Xing Zhang
    • Tao Wang
    • Qi‑Yi Zeng
  • View Affiliations

  • Published online on: February 26, 2018     https://doi.org/10.3892/etm.2018.5890
  • Pages: 3967-3975
  • Copyright: © Chen et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

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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April-2018
Volume 15 Issue 4

Print ISSN: 1792-0981
Online ISSN:1792-1015

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Spandidos Publications style
Chen GD, Zhang JL, Chen YT, Zhang JX, Wang T and Zeng QY: Insulin alleviates mitochondrial oxidative stress involving upregulation of superoxide dismutase 2 and uncoupling protein 2 in septic acute kidney injury. Exp Ther Med 15: 3967-3975, 2018
APA
Chen, G., Zhang, J., Chen, Y., Zhang, J., Wang, T., & Zeng, Q. (2018). Insulin alleviates mitochondrial oxidative stress involving upregulation of superoxide dismutase 2 and uncoupling protein 2 in septic acute kidney injury. Experimental and Therapeutic Medicine, 15, 3967-3975. https://doi.org/10.3892/etm.2018.5890
MLA
Chen, G., Zhang, J., Chen, Y., Zhang, J., Wang, T., Zeng, Q."Insulin alleviates mitochondrial oxidative stress involving upregulation of superoxide dismutase 2 and uncoupling protein 2 in septic acute kidney injury". Experimental and Therapeutic Medicine 15.4 (2018): 3967-3975.
Chicago
Chen, G., Zhang, J., Chen, Y., Zhang, J., Wang, T., Zeng, Q."Insulin alleviates mitochondrial oxidative stress involving upregulation of superoxide dismutase 2 and uncoupling protein 2 in septic acute kidney injury". Experimental and Therapeutic Medicine 15, no. 4 (2018): 3967-3975. https://doi.org/10.3892/etm.2018.5890