Low-Molecular-Weight Chitosan Attenuates Lipopolysaccharide-Induced Inflammation in IPEC-J2 Cells by Inhibiting the Nuclear Factor-κB Signalling Pathway

• Main Authors: Jiao Zhang, Jin Wan, Daiwen Chen, Bing Yu, Jun He
• Format: Article
• Language: English
• Published: MDPI AG 2021-01-01
• Series: Molecules
• Subjects: low-molecular-weight chitosan; lipopolysaccharide; inflammatory injury; cell apoptosis; intestinal epithelial cells
• Online Access: https://www.mdpi.com/1420-3049/26/3/569

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 (<i>p</i> < 0.05) the occludin abundance and decreased (<i>p</i> < 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 (<i>p</i> < 0.05) the expression levels of TNF receptor 1 (<i>TNFR1</i>) and TNFR-associated death domain and decreased (<i>p</i> < 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.