碳酸钙-2
TLR4型
化学
NF-κB
细胞因子
炎症
脂多糖
肿瘤坏死因子α
体外
壳聚糖
细胞生物学
药理学
分子生物学
信号转导
生物化学
免疫学
生物
作者
Jue Tu,Yinglei Xu,Jianqin Xu,Yun Ling,Yueqin Cai
标识
DOI:10.1016/j.ijbiomac.2016.02.015
摘要
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.
科研通智能强力驱动
Strongly Powered by AbleSci AI