Chitosan nanoparticles reduce LPS-induced inflammatory reaction via inhibition of NF-κB pathway in Caco-2 cells

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• 作者：Jue Tu^a ; ^{zheyu1114@126.com" class="auth_mail" title="E-mail the corresponding author} ; Yinglei Xu^b ; Jianqin Xu^a ; Yun Ling^a ; Yueqin Cai^a
• 关键词：CNP ; chitosan nanoparticles ; LPS ; lipopolysaccharide ; IBD ; inflammatory bowel diseases ; IEC ; intestinal epithelial cell ; TEER ; transepithelial electrical resistance ; TLR4 ; toll like receptor 4 ; NF- κB ; nuclear factor-kappa B ; IκB ; inhibitor of NF-κB ; TNF ; tumor necrosis factor ; MIF ; macrophage migration inhibitory factor ; MCP-1 ; monocyte chemoattractant protein-1
• 刊名：International Journal of Biological Macromolecules
• 出版年：2016
• 出版时间：May 2016
• 年：2016
• 卷：86
• 期：Complete
• 页码：848-856
• 全文大小：2142 K

文摘

Chitosan nanoparticles (CNP), an extensively oral-administered drug carrier, was investigated for the anti-inflammatory effects on LPS-inflamed Caco-2 cells and the relate mechanisms. CNP could alleviate the decrease of transepithelial electrical resistance (TEER) induced by LPS in Caco-2 monolayer, and significantly inhibit LPS-induced production of TNF-α, MIF, IL-8 and MCP-1 in a dose-dependent manner. PCR array assay revealed that CNP down-regulated the mRNA expression levels of TLR4 in LPS-inflamed Caco-2 cells. CNP was further showed to reduce cytoplasmic IκB-α degradation and nuclear NF-κB p65 levels in LPS-inflamed Caco-2 cells. These results suggested that CNP suppressed LPS-induced inflammatory response by decreasing permeability of intestinal epithelial monolayer and secretion of pro-inflammatory cytokine in Caco-2 cells, which were partially mediated by NF-κB signaling pathway.