5-Aminolevulinic acid exerts renoprotective effect via Nrf2 activation in murine rhabdomyolysis-induced acute kidney injury

Nephrology (Carlton). 2019 Jan;24(1):28-38. doi: 10.1111/nep.13189.

Abstract

Aim: Acute kidney injury (AKI) is associated with chronic kidney disease, as well as high mortality, but effective treatments for AKI are still lacking. A recent study reported the prevention of renal injury, such as ischemia-reperfusion injury, by 5-aminolevulinic acid (ALA), which induces an antioxidant effect. The current study aimed to investigate the effect of ALA in a rhabdomyolysis-induced mouse model of AKI created by intramuscular injection of 50% glycerol.

Methods: Rhabdomyolysis-induced AKI was induced by an intramuscular injection of glycerol (5 mL/kg body weight) into mice. Administration of ALA (30 mg/kg, by gavage) was started from 48 h before or 24 h after glycerol injection. The mice were sacrificed at 72 h after glycerol injection. The roles of nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1), which is one of the Nrf2-related antioxidants, were further investigated through in vivo and in vitro methods.

Results: 5-aminolevulinic acid markedly reduced renal dysfunction and tubular damage in mice with rhabdomyolysis-induced AKI. ALA administration decreased oxidative stress, macrophage infiltration, and inflammatory cytokines and apoptosis. The expression of Nrf2 was upregulated by ALA administration. However, administration of Zinc protoporphyrin-9 (ZnPPIX) to inhibit HO-1 activity did not abolish these improvements by ALA. The expression of Nrf2-associated antioxidant factors other than HO-1 was also increased.

Conclusion: These findings indicate that ALA exerts its antioxidant activity via Nrf2-associated antioxidant factors to provide a renoprotective effect against rhabdomyolysis-induced AKI.

Keywords: HO-1; NRF2; aminolevulinic acid; antioxidant effect; rhabdomyolysis-induced AKI.

MeSH terms

  • Acute Kidney Injury / chemically induced
  • Acute Kidney Injury / metabolism
  • Acute Kidney Injury / pathology
  • Acute Kidney Injury / prevention & control*
  • Aminolevulinic Acid / pharmacology*
  • Animals
  • Antioxidants / pharmacology*
  • Apoptosis / drug effects
  • Cells, Cultured
  • Cytokines / metabolism
  • Cytoprotection
  • Disease Models, Animal
  • Glycerol
  • Heme Oxygenase-1 / metabolism
  • Humans
  • Inflammation Mediators / metabolism
  • Kidney Tubules / drug effects*
  • Kidney Tubules / metabolism
  • Kidney Tubules / pathology
  • Macrophages / drug effects
  • Macrophages / metabolism
  • Macrophages / pathology
  • Male
  • Mice, Inbred C57BL
  • NF-E2-Related Factor 2 / agonists*
  • NF-E2-Related Factor 2 / genetics
  • NF-E2-Related Factor 2 / metabolism
  • Oxidative Stress / drug effects
  • Rhabdomyolysis / chemically induced
  • Rhabdomyolysis / metabolism
  • Rhabdomyolysis / pathology
  • Rhabdomyolysis / prevention & control*
  • Signal Transduction / drug effects

Substances

  • Antioxidants
  • Cytokines
  • Inflammation Mediators
  • NF-E2-Related Factor 2
  • Nfe2l2 protein, mouse
  • Aminolevulinic Acid
  • HMOX1 protein, human
  • Heme Oxygenase-1
  • Glycerol