Protocatechuic acid inhibits proliferation, migration and inflammatory response in rheumatoid arthritis fibroblast-like synoviocytes

AbstractRheumatoid arthritis (RA) is a chronic joint inflammatory disease that is closely associated with dysregulation of fibroblast-like synoviocytes (FLSs). Protocatechuic acid (PCA), a phenolic compound of anthocyanins, has been proven to possess anti-inflammatory activity. However, the role of...

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Main Authors: Huiqiang Wu, Jing Wang, Qing Zhao, Yanjie Ding, Bingyi Zhang, Lingli Kong
Format: Article
Language:English
Published: Taylor & Francis Group 2020-01-01
Series:Artificial Cells, Nanomedicine, and Biotechnology
Subjects:
Online Access:https://www.tandfonline.com/doi/10.1080/21691401.2020.1776307
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author Huiqiang Wu
Jing Wang
Qing Zhao
Yanjie Ding
Bingyi Zhang
Lingli Kong
author_facet Huiqiang Wu
Jing Wang
Qing Zhao
Yanjie Ding
Bingyi Zhang
Lingli Kong
author_sort Huiqiang Wu
collection DOAJ
description AbstractRheumatoid arthritis (RA) is a chronic joint inflammatory disease that is closely associated with dysregulation of fibroblast-like synoviocytes (FLSs). Protocatechuic acid (PCA), a phenolic compound of anthocyanins, has been proven to possess anti-inflammatory activity. However, the role of PCA in RA has not been investigated. In the present study, we aimed to explore the effects of PCA on the RA-FLSs. The results showed that PCA suppressed the proliferation, invasion, and migration of RA-FLSs in a dose-dependent manner. PCA treatment also inhibited the expressions of matrix metalloproteinase (MMP)-3 and MMP-13, as well as the secretion of inflammatory cytokines including TNF-α, IL-1β, IL-6 in RA-FLSs. Moreover, cell apoptosis of RA-FLSs was significantly induced by PCA treatment. PCA was found to repress the activation of NF-κB signalling, which was evidenced by the decreased expression of p-p65 and increased expression of IκBα. Furthermore, PCA significantly decreased the phosphorylation levels of Akt and mTOR in RA-FLSs. In conclusion, the results indicated that PCA exhibited an inhibitory effect on RA-FLSs via inhibiting the NF-κB and Akt/mTOR signalling pathways. These findings supported the concept that PCA might be a therapeutic agent for RA treatment.
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spelling doaj.art-cf05839604844a29b3d401035fb3a8402023-07-03T14:04:55ZengTaylor & Francis GroupArtificial Cells, Nanomedicine, and Biotechnology2169-14012169-141X2020-01-0148196997610.1080/21691401.2020.1776307Protocatechuic acid inhibits proliferation, migration and inflammatory response in rheumatoid arthritis fibroblast-like synoviocytesHuiqiang Wu0Jing Wang1Qing Zhao2Yanjie Ding3Bingyi Zhang4Lingli Kong5Department of Rheumatology and Immunology, Huaihe Hospital, Henan University, Kaifeng, People’s Republic of ChinaDepartment of Rheumatology and Immunology, Huaihe Hospital, Henan University, Kaifeng, People’s Republic of ChinaDepartment of Rheumatology and Immunology, Huaihe Hospital, Henan University, Kaifeng, People’s Republic of ChinaDepartment of Rheumatology and Immunology, Huaihe Hospital, Henan University, Kaifeng, People’s Republic of ChinaDepartment of Rheumatology and Immunology, Huaihe Hospital, Henan University, Kaifeng, People’s Republic of ChinaDepartment of Rheumatology and Immunology, Huaihe Hospital, Henan University, Kaifeng, People’s Republic of ChinaAbstractRheumatoid arthritis (RA) is a chronic joint inflammatory disease that is closely associated with dysregulation of fibroblast-like synoviocytes (FLSs). Protocatechuic acid (PCA), a phenolic compound of anthocyanins, has been proven to possess anti-inflammatory activity. However, the role of PCA in RA has not been investigated. In the present study, we aimed to explore the effects of PCA on the RA-FLSs. The results showed that PCA suppressed the proliferation, invasion, and migration of RA-FLSs in a dose-dependent manner. PCA treatment also inhibited the expressions of matrix metalloproteinase (MMP)-3 and MMP-13, as well as the secretion of inflammatory cytokines including TNF-α, IL-1β, IL-6 in RA-FLSs. Moreover, cell apoptosis of RA-FLSs was significantly induced by PCA treatment. PCA was found to repress the activation of NF-κB signalling, which was evidenced by the decreased expression of p-p65 and increased expression of IκBα. Furthermore, PCA significantly decreased the phosphorylation levels of Akt and mTOR in RA-FLSs. In conclusion, the results indicated that PCA exhibited an inhibitory effect on RA-FLSs via inhibiting the NF-κB and Akt/mTOR signalling pathways. These findings supported the concept that PCA might be a therapeutic agent for RA treatment.https://www.tandfonline.com/doi/10.1080/21691401.2020.1776307Rheumatoid arthritis (RA)fibroblast-like synoviocytes (FLSs)PCAinflammationNF-κB signalling pathwayAkt/mTOR pathway
spellingShingle Huiqiang Wu
Jing Wang
Qing Zhao
Yanjie Ding
Bingyi Zhang
Lingli Kong
Protocatechuic acid inhibits proliferation, migration and inflammatory response in rheumatoid arthritis fibroblast-like synoviocytes
Artificial Cells, Nanomedicine, and Biotechnology
Rheumatoid arthritis (RA)
fibroblast-like synoviocytes (FLSs)
PCA
inflammation
NF-κB signalling pathway
Akt/mTOR pathway
title Protocatechuic acid inhibits proliferation, migration and inflammatory response in rheumatoid arthritis fibroblast-like synoviocytes
title_full Protocatechuic acid inhibits proliferation, migration and inflammatory response in rheumatoid arthritis fibroblast-like synoviocytes
title_fullStr Protocatechuic acid inhibits proliferation, migration and inflammatory response in rheumatoid arthritis fibroblast-like synoviocytes
title_full_unstemmed Protocatechuic acid inhibits proliferation, migration and inflammatory response in rheumatoid arthritis fibroblast-like synoviocytes
title_short Protocatechuic acid inhibits proliferation, migration and inflammatory response in rheumatoid arthritis fibroblast-like synoviocytes
title_sort protocatechuic acid inhibits proliferation migration and inflammatory response in rheumatoid arthritis fibroblast like synoviocytes
topic Rheumatoid arthritis (RA)
fibroblast-like synoviocytes (FLSs)
PCA
inflammation
NF-κB signalling pathway
Akt/mTOR pathway
url https://www.tandfonline.com/doi/10.1080/21691401.2020.1776307
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