Rheumatoid 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.

中文翻译：

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原儿茶酸抑制类风湿关节炎成纤维细胞样滑膜细胞的增殖，迁移和炎症反应。

类风湿关节炎（RA）是一种慢性关节炎，与成纤维样滑膜细胞（FLSs）失调密切相关。花青素的酚类化合物原儿茶酸（PCA）已被证明具有抗炎活性。但是，尚未研究PCA在RA中的作用。在本研究中，我们旨在探讨PCA对RA-FLS的影响。结果表明，PCA以剂量依赖性方式抑制RA-FLS的增殖，侵袭和迁移。PCA处理还抑制RA-FLS中基质金属蛋白酶（MMP）-3和MMP-13的表达，以及TNF-α，IL-1β，IL-6等炎性细胞因子的分泌。而且，通过PCA处理显着诱导了RA-FLS的细胞凋亡。发现PCA可抑制NF-κB信号的激活，p-p65的表达减少和IκBα的表达增加证明了这一点。此外，PCA显着降低了RA-FLS中Akt和mTOR的磷酸化水平。总之，结果表明PCA通过抑制NF-κB和Akt / mTOR信号通路对RA-FLSs表现出抑制作用。这些发现支持了PCA可能是RA治疗的治疗剂这一概念。