Tectoridin exhibits anti-rheumatoid arthritis activity through the inhibition of the inflammatory response and the MAPK pathway in vivo and in vitro

关节炎 化学 炎症 体内 MAPK/ERK通路 类风湿性关节炎 滑膜 肿瘤坏死因子α 成纤维细胞 p38丝裂原活化蛋白激酶 免疫学 药理学 医学 信号转导 体外 生物 生物化学 生物技术
作者
Qiuxia Huang,Xin Xiao,Jinjin Yu,Yajie Yang,Jiabao Yu,Yang Liu,Huixin Song,Tengfei Han,Dezhu Zhang,Xiaofeng Niu,Weifeng Li
出处
期刊:Archives of Biochemistry and Biophysics [Elsevier BV]
卷期号:727: 109328-109328 被引量:17
标识
DOI:10.1016/j.abb.2022.109328
摘要

Rheumatoid arthritis (RA) is a chronic inflammatory disease characterized by inflammation infiltration of the synovial tissues and the fibroblast-like synoviocytes. Tectoridin is a botanical active ingredient with anti-inflammatory properties. In this study, the anti-arthritic effects of tectoridin and its mechanism of action are examined in TNF-α-induced human fibroblast-like synovial cells (HFLSs cells) and complete Freund's adjuvant (CFA)-stimulated arthritic mice. Arthritis progression was evaluated via bodyweight, hind paw swelling, organ index, and synovial pathology. IL-1β, IL-6 and other pro-inflammatory factors concentrations, and the expression of MAPK pathway proteins in HFLSs cells and arthritic mice were measured using ELISA and western blotting. Results showed that tectoridin significantly decreased the swelling of the paws and joints as well as the increased immune organ index within CFA-induced arthritic mice. Histopathological analysis showed that tectoridin alleviated the lesions of ankle joints and synovial tissues induced by CFA. Secretion of pro-inflammatory cytokines in TNF-α-induced HFLSs cells and CFA-stimulated arthritic mice were also abated by tectoridin. Similarly, the presence of tectoridin significantly inhibited the abnormal phosphorylation levels of ERK, JNK, and p38 in vivo and in vitro. All those results highlighted that tectoridin exhibits anti-arthritis effects by inhibiting MAPK-mediated inflammatory responses.
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