雷公藤甲素
车站3
关节炎
PTEN公司
炎症
流式细胞术
脾脏
癌症研究
肿瘤坏死因子α
下调和上调
信号转导
细胞凋亡
化学
医学
免疫学
PI3K/AKT/mTOR通路
生物
细胞生物学
基因
生物化学
作者
Yao Huang,Xin Ba,Hui Wang,Pan Shen,Liang Han,Weiji Lin,Jiahui Yan,Zhe Chen,Shenghao Tu
摘要
This study aimed to investigate the effects of triptolide (TP) on collagen-induced arthritis (CIA) mice and the related mechanisms.CIA mice were administered TP for 35 days. Mouse ankle joints and serum antibodies and cytokines were examined to assess the therapeutic effects of TP. The ratios of Treg, Th1 and Th17 cells were measured by flow cytometry and RT-qPCR. Reverse docking was used to characterize the binding modes of TP against target proteins. The expression of the STAT3 pathway in CIA mice was evaluated by western blotting and immunofluorescence staining. Mouse spleen lymphocytes were extracted, and the expression of the STAT3 pathway after IL-6 stimulation was analysed.TP could significantly alleviate joint swelling, reduce bone destruction and downregulate serum inflammation levels. TP improved the imbalance of Treg/Th17 cells in CIA mice. TP could form stable complexes with target proteins. TP significantly inhibited the activation of the JAK/PTEN-STAT3 pathway in mice. Moreover, TP regulated the activation of the JAK1/2-STAT3 signalling pathway in mouse spleen lymphocytes under inflammatory stimulation.TP can inhibit inflammation and alleviate bone destruction in CIA mice. The underlying mechanism is related to the regulation of the imbalance of Treg/Th17 cells through the JAK/PTEN-STAT3 pathway.
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