N-acetylcysteine suppresses colistimethate sodium-induced nephrotoxicity via activation of SOD2, eNOS, and MMP3

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Bahadir Ceylan1, Mehmet Ozansoy2, Ülkan Kılıç3

  • 1a Department of Infectious Diseases and Clinical Microbiology, Faculty of Medicine , Istanbul Medipol University , Istanbul , Turkey.

Renal Failure
|July 24, 2018
PubMed
Abstract

Insights

N-acetylcysteine (NAC) protects against colistin-induced nephrotoxicity by restoring key molecular markers in rats. This study reveals NAC’s potential to mitigate kidney damage from colistin treatment.

Area of Science:

  • Nephrology
  • Pharmacology
  • Molecular Biology

Background:

  • Colistimethate sodium (colistin) is crucial for treating multidrug-resistant Gram-negative bacterial infections.
  • Colistin use is limited by significant nephrotoxicity, necessitating research into its mechanisms and potential countermeasures.
  • N-acetylcysteine (NAC) is an antioxidant with potential protective effects against drug-induced organ damage.

Purpose of the Study:

  • To elucidate the molecular pathways underlying colistin-induced nephrotoxicity.
  • To evaluate the efficacy of N-acetylcysteine (NAC) in preventing or mitigating colistin-induced kidney damage.

Main Methods:

  • Wistar rats were assigned to control, colistin, NAC, or colistin-NAC co-treatment groups.
  • Biochemical markers (serum creatinine, urine NAG) and renal tissue parameters (histology, apoptosis, oxidant/antioxidant status, eNOS, SOD2, MMP3 expression) were assessed.
  • Statistical analysis was performed to compare outcomes between groups.

Main Results:

  • Colistin treatment significantly elevated serum creatinine and urine NAG levels, indicating kidney injury.
  • Colistin induced increased renal histological damage and apoptosis, which were significantly reduced by NAC co-treatment.
  • Colistin decreased the expression of endothelial nitric oxide synthase (eNOS), superoxide dismutase 2 (SOD2), and matrix metalloproteinase 3 (MMP3), while NAC reversed these changes.

Conclusions:

  • N-acetylcysteine (NAC) effectively prevented colistin-induced nephrotoxicity in a rat model.
  • The protective mechanism involves the upregulation of SOD2, eNOS, and MMP3 expression by NAC.
  • NAC represents a promising therapeutic strategy to mitigate colistin-associated kidney injury.
Keywords:
Antioxidantcolistinnephrotoxicityrat modelreactive oxygen species

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