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多糖对感染的RAW264.7巨噬细胞炎症反应的抑制作用

Inhibitory Effects of Polysaccharide on Inflammatory Response in Infected RAW264.7 Macrophages.

作者信息

Yan Kexin, Zhou Hongyuan, Wang Meng, Li Haitao, Sang Rui, Ge Bingjie, Zhao Xin, Li Chunting, Wang Wei, Zhang Xuemei

机构信息

Agricultural College of Yanbian University, Gongyuan Street, Yanji, Jilin 133002, China.

Institute of Special Wild Economic Animals and Plants, Chinese Academy of Agricultural Sciences, Juye Street, Changchun, Jilin 132109, China.

出版信息

Evid Based Complement Alternat Med. 2021 Dec 29;2021:2245496. doi: 10.1155/2021/2245496. eCollection 2021.

DOI:10.1155/2021/2245496
PMID:35003292
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8731277/
Abstract

Our previous reports have shown that polysaccharide (IOP) has protective effects against () infection . The aim of the present research is to explore the anti-inflammatory effects of IOP and its mechanism in RAW264.7 macrophages infected by . In this study, it is indicated that IOP decreased the excessive secretion of inflammatory cytokines tumor necrosis factor- (TNF-), interferon- (IFN-), interleukin-1 (IL-1), IL-4, and IL-6 in -infected RAW264.7 macrophages. IOP effectively suppressed the mRNA expression of these cytokines and chemokines monocyte chemoattractant protein-1 (MCP-1) and macrophage inflammatory protein-1 (MIP-1). Moreover, IOP inhibited the phosphorylation of inhibitor kappa B kinase / (IKK/), inhibitor B (IB), p65 in nuclear factor-kappa B (NF-B) signaling pathway and p38, c-Jun N-terminal kinase (JNK), and extracellular signal-regulated kinase 1/2 (ERK1/2) in mitogen-activated protein kinases (MAPKs) signaling pathway. Meantime, IOP prevented NF-B p65 and c-Jun translocation from the cytoplasm to the nucleus. Further, IOP downregulated the protein expression of toll-like receptor 2 (TLR2) and TLR4 in -infected RAW264.7 macrophages. The above results suggest that IOP can inhibit the inflammatory response infected with via regulating TLR2/TLR4-NF-B/MAPKs pathways and exerting its anti- role .

摘要

我们之前的报告表明，多糖（IOP）对（）感染具有保护作用。本研究的目的是探讨IOP在被感染的RAW264.7巨噬细胞中的抗炎作用及其机制。在本研究中，结果表明IOP可减少被感染的RAW264.7巨噬细胞中炎性细胞因子肿瘤坏死因子-（TNF-）、干扰素-（IFN-）、白细胞介素-1（IL-1）、IL-4和IL-6的过度分泌。IOP有效抑制了这些细胞因子和趋化因子单核细胞趋化蛋白-1（MCP-1）和巨噬细胞炎性蛋白-1（MIP-1）的mRNA表达。此外，IOP抑制了核因子-κB（NF-κB）信号通路中抑制因子κB激酶/（IKK/）、抑制因子B（IκB）、p65的磷酸化以及丝裂原活化蛋白激酶（MAPKs）信号通路中p38、c-Jun氨基末端激酶（JNK）和细胞外信号调节激酶1/2（ERK1/2）的磷酸化。同时，IOP阻止了NF-κB p65和c-Jun从细胞质向细胞核的转位。此外，IOP下调了被感染的RAW264.7巨噬细胞中Toll样受体2（TLR2）和TLR4的蛋白表达。上述结果表明，IOP可通过调节TLR2/TLR4-NF-κB/MAPKs通路抑制感染后的炎症反应并发挥其抗炎作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a9ff/8731277/c326e33d8fd9/ECAM2021-2245496.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a9ff/8731277/aa9d13aabee7/ECAM2021-2245496.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a9ff/8731277/5411527ee149/ECAM2021-2245496.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a9ff/8731277/ed4164b17e21/ECAM2021-2245496.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a9ff/8731277/5005389dac73/ECAM2021-2245496.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a9ff/8731277/7100cc876689/ECAM2021-2245496.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a9ff/8731277/c326e33d8fd9/ECAM2021-2245496.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a9ff/8731277/aa9d13aabee7/ECAM2021-2245496.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a9ff/8731277/5411527ee149/ECAM2021-2245496.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a9ff/8731277/ed4164b17e21/ECAM2021-2245496.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a9ff/8731277/5005389dac73/ECAM2021-2245496.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a9ff/8731277/7100cc876689/ECAM2021-2245496.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a9ff/8731277/c326e33d8fd9/ECAM2021-2245496.006.jpg

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