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
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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