Abstract
Low-molecular-weight chitosan (LMWC), a product of chitosan deacetylation, possesses anti-inflammatory effects. In the present study, a porcine small intestinal epithelial cell line, IPEC-J2, was used to assess the protective effects of LMWC on lipopolysaccharide (LPS)-induced intestinal epithelial cell injury. IPEC-J2 cells were pretreated with or without LMWC (400 μg/mL) in the presence or absence of LPS (5 μg/mL) for 6 h. LMWC pretreatment increased (p < 0.05) the occludin abundance and decreased (p < 0.05) the tumour necrosis factor-α (TNF-α) production, apoptosis rate and cleaved cysteinyl aspartate-specific protease-3 (caspase-3) and -8 contents in LPS-treated IPEC-J2 cells. Moreover, LMWC pretreatment downregulated (p < 0.05) the expression levels of TNF receptor 1 (TNFR1) and TNFR-associated death domain and decreased (p < 0.05) the nuclear and cytoplasmic abundance of nuclear factor-κB (NF-κB) p65 in LPS-stimulated IPEC-J2 cells. These results suggest that LMWC exerts a mitigation effect on LPS-induced intestinal epithelial cell damage by suppressing TNFR1-mediated apoptosis and decreasing the production of proinflammatory cytokines via the inhibition of NF-κB signalling pathway.
Highlights
Tight junctions are an important part of the intestinal epithelial barrier; they are located in the apical membrane and basolateral surface of intestinal epithelial cells and are responsible for cell–cell adhesion, polarity and forming a permeability barrier for intercellular solute transport [21,22,23,24]
Occludin is involved in the regulation of intermembrane diffusion and paracellular diffusion of small molecules; it has functional importance in maintaining the integrity of the intestinal epithelial barrier [25]
We found that LPS decreased the occludin abundance in IPEC-J2 cells, while Low-molecular-weight chitosan (LMWC) pretreatment restored the LPS-induced reduction in the occludin abundance
Summary
Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations. The secreted proinflammatory cytokines can expedite the apoptosis of intestinal epithelial cells and further damage the intestinal barrier integrity [6,7]. Dietary treatments targeted at reducing the intestinal proinflammatory cytokine production and epithelial cell apoptosis could contribute to improving the intestinal barrier integrity. Chitosan extracted from chitin has a high molecular weight and poor solubility, which greatly limit its applications To address these undesirable properties, more active forms, such as chitosan oligosaccharide and low-molecular-weight chitosan (LMWC), have been generated [13]. Small the present study aimed tocell assess injuryonand its potential mechanisms a porcine intestinal epithelial line, the protective effects of LMWC on LPS-induced intestinal epithelial cell injury and its IPEC-J2. Potential mechanisms using a porcine small intestinal epithelial cell line, IPEC-J2
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