Wilforlide A ameliorates the progression of rheumatoid arthritis by inhibiting M1 macrophage polarization

Rheumatoid arthritis (RA) is an autoimmune disease with increased M1 macrophages. The classical activated M1 macrophages produce various cytokines to control inflammation. Wilforlide A is a natural product that displays anti-inflammatory activities. However, the effect of Wilforlide A on RA progress...

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Autores principales:	Yunxiang Cao, Jian Liu, Chuanbing Huang, Yanhong Tao, Yuan Wang, Xi Chen, Dan Huang
Formato:	article
Lenguaje:	EN
Publicado:	Elsevier 2022
Materias:	Wilforlide A Rheumatoid arthritis Macrophage polarization TLR4 NF-κB Therapeutics. Pharmacology RM1-950
Acceso en línea:	https://doaj.org/article/e73b91a2e1464bdb8be674f13fea292a
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spelling	oai:doaj.org-article:e73b91a2e1464bdb8be674f13fea292a2021-11-20T04:57:28ZWilforlide A ameliorates the progression of rheumatoid arthritis by inhibiting M1 macrophage polarization1347-861310.1016/j.jphs.2021.10.005https://doaj.org/article/e73b91a2e1464bdb8be674f13fea292a2022-01-01T00:00:00Zhttp://www.sciencedirect.com/science/article/pii/S1347861321001006https://doaj.org/toc/1347-8613Rheumatoid arthritis (RA) is an autoimmune disease with increased M1 macrophages. The classical activated M1 macrophages produce various cytokines to control inflammation. Wilforlide A is a natural product that displays anti-inflammatory activities. However, the effect of Wilforlide A on RA progression and the potential mechanisms are unclear. Herein, the collagen-induced arthritis (CIA) mouse was used as an experimental model of RA. The administration of Wilforlide A reduced clinical scores, joint swelling and histological damage in ankle joints of RA mice. The secreted pro-inflammatory factors (MCP1, GM-CSF and M-CSF) and M1 biomarker iNOS in synovium were inhibited by Wilforlide A. In vitro, macrophages deriving from THP-1 cells were stimulated with LPS/IFN-γ to mimic M1 polarization. Similarly, Wilforlide A blocked macrophages polarizing towards M1 subsets. The in vitro results demonstrated that Wilforlide A suppressed LPS/IFN-γ-induced TLR4 upregulation, IκBα degradation and NF-κB p65 activation. In addition, TAK242 (a TLR4 inhibitor) treatment caused a similar inhibitory effect on M1 polarization with Wilforlide A, whereas it was less than the combination of TAK242 and Wilforlide A. Therefore, this work supports that Wilforlide A ameliorates M1 macrophage polarization in RA, which is partially mediated by TLR4/NF-κB signaling pathway inactivation.Yunxiang CaoJian LiuChuanbing HuangYanhong TaoYuan WangXi ChenDan HuangElsevierarticleWilforlide ARheumatoid arthritisMacrophage polarizationTLR4NF-κBTherapeutics. PharmacologyRM1-950ENJournal of Pharmacological Sciences, Vol 148, Iss 1, Pp 116-124 (2022)
institution	DOAJ
collection	DOAJ
language	EN
topic	Wilforlide A Rheumatoid arthritis Macrophage polarization TLR4 NF-κB Therapeutics. Pharmacology RM1-950
spellingShingle	Wilforlide A Rheumatoid arthritis Macrophage polarization TLR4 NF-κB Therapeutics. Pharmacology RM1-950 Yunxiang Cao Jian Liu Chuanbing Huang Yanhong Tao Yuan Wang Xi Chen Dan Huang Wilforlide A ameliorates the progression of rheumatoid arthritis by inhibiting M1 macrophage polarization
description	Rheumatoid arthritis (RA) is an autoimmune disease with increased M1 macrophages. The classical activated M1 macrophages produce various cytokines to control inflammation. Wilforlide A is a natural product that displays anti-inflammatory activities. However, the effect of Wilforlide A on RA progression and the potential mechanisms are unclear. Herein, the collagen-induced arthritis (CIA) mouse was used as an experimental model of RA. The administration of Wilforlide A reduced clinical scores, joint swelling and histological damage in ankle joints of RA mice. The secreted pro-inflammatory factors (MCP1, GM-CSF and M-CSF) and M1 biomarker iNOS in synovium were inhibited by Wilforlide A. In vitro, macrophages deriving from THP-1 cells were stimulated with LPS/IFN-γ to mimic M1 polarization. Similarly, Wilforlide A blocked macrophages polarizing towards M1 subsets. The in vitro results demonstrated that Wilforlide A suppressed LPS/IFN-γ-induced TLR4 upregulation, IκBα degradation and NF-κB p65 activation. In addition, TAK242 (a TLR4 inhibitor) treatment caused a similar inhibitory effect on M1 polarization with Wilforlide A, whereas it was less than the combination of TAK242 and Wilforlide A. Therefore, this work supports that Wilforlide A ameliorates M1 macrophage polarization in RA, which is partially mediated by TLR4/NF-κB signaling pathway inactivation.
format	article
author	Yunxiang Cao Jian Liu Chuanbing Huang Yanhong Tao Yuan Wang Xi Chen Dan Huang
author_facet	Yunxiang Cao Jian Liu Chuanbing Huang Yanhong Tao Yuan Wang Xi Chen Dan Huang
author_sort	Yunxiang Cao
title	Wilforlide A ameliorates the progression of rheumatoid arthritis by inhibiting M1 macrophage polarization
title_short	Wilforlide A ameliorates the progression of rheumatoid arthritis by inhibiting M1 macrophage polarization
title_full	Wilforlide A ameliorates the progression of rheumatoid arthritis by inhibiting M1 macrophage polarization
title_fullStr	Wilforlide A ameliorates the progression of rheumatoid arthritis by inhibiting M1 macrophage polarization
title_full_unstemmed	Wilforlide A ameliorates the progression of rheumatoid arthritis by inhibiting M1 macrophage polarization
title_sort	wilforlide a ameliorates the progression of rheumatoid arthritis by inhibiting m1 macrophage polarization
publisher	Elsevier
publishDate	2022
url	https://doaj.org/article/e73b91a2e1464bdb8be674f13fea292a
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Wilforlide A ameliorates the progression of rheumatoid arthritis by inhibiting M1 macrophage polarization

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