Fasting reduces oxidative stress, mitochondrial dysfunction and fibrosis induced by renal ischemia-reperfusion injury

Free Radic Biol Med. 2019 May 1:135:60-67. doi: 10.1016/j.freeradbiomed.2019.02.018. Epub 2019 Feb 25.

Abstract

Food deprivation protects against ischemia-reperfusion (IR) injury through unknown mechanisms. In an experimental rat model of acute IR injury, we found that preoperative fasting for 3 days protects rats from tubular damage and renal functional decline by increasing antioxidant protection independently of the NF-E2-related factor 2 (Nrf2), and by maintaining mitochondrial morphology and function. In addition, further analysis revealed that fasting protects against tubulointerstitial fibrosis. In summary, our results point out to fasting as a robust nutritional intervention to limit oxidative stress and mitochondrial dysfunction in early acute kidney injury and also to promote long-term protection against fibrosis.

Keywords: Acute kidney injury; Chronic kidney disease; Fasting; Fibrosis; Ischemia-reperfusion injury; Mitochondrial dysfunction; Oxidative stress.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acute Kidney Injury / diet therapy*
  • Acute Kidney Injury / genetics
  • Acute Kidney Injury / metabolism
  • Acute Kidney Injury / pathology
  • Animals
  • Antioxidants / metabolism
  • Fasting / metabolism
  • Fibrosis / diet therapy
  • Fibrosis / metabolism
  • Fibrosis / pathology
  • Food Deprivation
  • Humans
  • Kidney / injuries
  • Kidney / metabolism*
  • Kidney / pathology
  • Kidney Tubules / metabolism
  • Kidney Tubules / pathology
  • Malondialdehyde / metabolism
  • Mitochondria / metabolism
  • NF-E2-Related Factor 2 / genetics*
  • NF-E2-Related Factor 2 / metabolism
  • Oxidative Stress / genetics
  • Rats
  • Reperfusion Injury / diet therapy*
  • Reperfusion Injury / genetics
  • Reperfusion Injury / metabolism
  • Reperfusion Injury / pathology

Substances

  • Antioxidants
  • NF-E2-Related Factor 2
  • Nfe2l2 protein, rat
  • Malondialdehyde