Abstract
Oxidative stress in the small intestinal epithelium is a major cause of barrier malfunction and failure to regenerate. This study presents a functional in vitro model using the porcine small intestinal epithelial cell line IPEC-J2 to examine the effects of oxidative stress and to estimate the antioxidant and regenerative potential of Trolox, ascorbic acid and glutathione monoethyl ester. Hydrogen peroxide and diethyl maleate affected the tight junction (zona occludens-1) distribution, significantly increased intracellular oxidative stress (CM-H2DCFDA) and decreased the monolayer integrity (transepithelial electrical resistance and FD-4 permeability), viability (neutral red) and wound healing capacity (scratch assay). Trolox (2 mM) and 1 mM ascorbic acid pre-treatment significantly reduced intracellular oxidative stress, increased wound healing capacity and reduced FD-4 permeability in oxidatively stressed IPEC-J2 cell monolayers. All antioxidant pre-treatments increased transepithelial electrical resistance and viability only in diethyl maleate-treated cells. Glutathione monoethyl ester (10 mM) pre-treatment significantly decreased intracellular oxidative stress and monolayer permeability only in diethyl maleate-treated cells. These data demonstrate that the IPEC-J2 oxidative stress model is a valuable tool to screen antioxidants before validation in piglets.
Highlights
Oxidative stress is considered one of the key players in malabsorption and inflammation of the gastrointestinal tract (GIT) as seen in necrotizing enterocolitis (NEC) [1], celiac disease [2], inflammatory bowel disease (IBD) [3] and Crohn’s disease [4]
Pre-treatment with either 2 mM Trolox or 1 mM ascorbic acid prior to the 0.5 mM H2O2 treatment significantly reduced the intracellular oxidative stress assessed by the mean fluorescence intensity (MFI) (p
This research showed that both 0.5 mM H2O2 and 4 mM diethyl maleate (DEM) cause extensive intracellular oxidative stress in IPEC-J2 cells
Summary
Oxidative stress is considered one of the key players in malabsorption and inflammation of the gastrointestinal tract (GIT) as seen in necrotizing enterocolitis (NEC) [1], celiac disease [2], inflammatory bowel disease (IBD) [3] and Crohn’s disease [4]. Oxidative stress has been shown to be one of the underlying pathophysiological mechanisms in a variety of diseases [5,6,7,8,9]. Trolox and Ascorbic Acid Reduce Oxidative Stress in the IPEC-J2 Cells
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