N-Acetyl-L-cysteine Protects the Enterocyte against Oxidative Damage by Modulation of Mitochondrial Function

Mediators Inflamm. 2016:2016:8364279. doi: 10.1155/2016/8364279. Epub 2016 Nov 27.

Abstract

The neonatal small intestine is susceptible to damage caused by oxidative stress. This study aimed to evaluate the protective role of antioxidant N-acetylcysteine (NAC) in intestinal epithelial cells against oxidative damage induced by H2O2. IPEC-J2 cells were cultured in DMEM-H with NAC and H2O2. After 2-day incubation, IPEC-J2 cells were collected for analysis of DNA synthesis, antioxidation capacity, mitochondrial respiration, and cell apoptosis. The results showed that H2O2 significantly decreased (P < 0.05) proliferation rate, mitochondrial respiration, and antioxidation capacity and increased cell apoptosis and the abundance of associated proteins, including cytochrome C, Bcl-XL, cleaved caspase-3, and total caspase-3. NAC supplementation remarkably increased (P < 0.05) proliferation rate, antioxidation capacity, and mitochondrial bioenergetics but decreased cell apoptosis. These findings indicate that NAC might rescue the intestinal injury induced by H2O2.

MeSH terms

  • Acetylcysteine / pharmacology*
  • Animals
  • Antioxidants / chemistry
  • Apoptosis / drug effects
  • Caspase 3 / metabolism
  • Cell Proliferation
  • Cell Survival
  • Cytochromes c / metabolism
  • DNA / metabolism
  • Enterocytes / drug effects*
  • Flow Cytometry
  • Free Radical Scavengers / metabolism
  • Hydrogen Peroxide / chemistry
  • Mitochondria / drug effects
  • Mitochondria / metabolism*
  • Oxidative Stress*
  • Swine
  • bcl-X Protein / metabolism

Substances

  • Antioxidants
  • Free Radical Scavengers
  • bcl-X Protein
  • Cytochromes c
  • DNA
  • Hydrogen Peroxide
  • Caspase 3
  • Acetylcysteine