Pretreatment with Cholecalciferol Alleviates Renal Cellular Stress Response during Ischemia/Reperfusion-Induced Acute Kidney Injury

Oxid Med Cell Longev. 2019 Mar 25:2019:1897316. doi: 10.1155/2019/1897316. eCollection 2019.

Abstract

Background: Cellular stress is involved in ischemia/reperfusion- (I/R-) induced acute kidney injury (AKI). This study is aimed at investigating the effects of pretreatment with cholecalciferol on renal oxidative stress and endoplasmic reticulum (ER) stress during I/R-induced AKI.

Methods: I/R-induced AKI was established by cross-clamping renal pedicles for 90 minutes and then reperfusion. In the Chol + I/R group, mice were orally administered with three doses of cholecalciferol (25 μg/kg) at 1, 24, and 48 h before ischemia. Renal cellular stress and kidney injury were measured at different time points after reperfusion.

Results: I/R-induced AKI was alleviated in mice pretreated with cholecalciferol. In addition, I/R-induced renal cell apoptosis, as determined by TUNEL, was suppressed by cholecalciferol. Additional experiment showed that I/R-induced upregulation of renal GRP78 and CHOP was inhibited by cholecalciferol. I/R-induced renal IRE1α and eIF2α phosphorylation was attenuated by cholecalciferol. Moreover, I/R-induced renal GSH depletion, lipid peroxidation, and protein nitration were blocked in mice pretreated with cholecalciferol. I/R-induced upregulation of renal NADPH oxidases, such as p47phox, gp91phox, and nox4, was inhibited by cholecalciferol. I/R-induced upregulation of heme oxygenase- (HO-) 1, gshpx and gshrd, was attenuated in mice pretreated with cholecalciferol.

Conclusions: Pretreatment with cholecalciferol protects against I/R-induced AKI partially through suppressing renal cellular stress response.

MeSH terms

  • Acute Kidney Injury / etiology*
  • Acute Kidney Injury / pathology*
  • Animals
  • Antioxidants / metabolism
  • Apoptosis / drug effects
  • Cholecalciferol / pharmacology*
  • Endoplasmic Reticulum Chaperone BiP
  • Endoplasmic Reticulum Stress / drug effects*
  • Glutathione / metabolism
  • Kidney / drug effects
  • Kidney / pathology*
  • Lipid Peroxidation / drug effects
  • Male
  • Mice, Inbred ICR
  • NADPH Oxidases / metabolism
  • Oxidative Stress / drug effects*
  • Receptors, Calcitriol / metabolism
  • Reperfusion Injury / complications*
  • Signal Transduction / drug effects
  • Up-Regulation / drug effects

Substances

  • Antioxidants
  • Endoplasmic Reticulum Chaperone BiP
  • Hspa5 protein, mouse
  • Receptors, Calcitriol
  • Cholecalciferol
  • NADPH Oxidases
  • Glutathione