Investigating the molecular mechanism of epimedium herb in treating rheumatoid arthritis through network pharmacology, molecular docking, and experimental validation

被引:0
|
作者
Ding, Chunhui [1 ]
Liu, Qingyang [2 ]
You, Xiaohong [1 ]
Yuan, Jianming [2 ]
Xia, Jinjun [2 ]
Tan, Yuan [2 ]
Hu, Yunxia [3 ]
Wang, Qiubo [2 ]
机构
[1] Soochow Univ, Wuxi Peoples Hosp 9, Dept Pharm, 999 Liang Xi Rd, Wuxi 214000, Jiangsu, Peoples R China
[2] Soochow Univ, Wuxi Peoples Hosp 9, Dept Clin Lab, Wuxi 214000, Jiangsu, Peoples R China
[3] Nanjing Med Univ, Wuxi Peoples Hosp, Dept Rheumatol & Immunol, Wuxi 214000, Jiangsu, Peoples R China
关键词
Epimedium herb; Rheumatoid arthritis; Network pharmacology; Fibroblast-like synoviocytes; Collagen-induced arthritis; MIGRATION; DIAGNOSIS; INVASION;
D O I
10.1007/s11030-024-11019-z
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
This study attempted to explore the molecular mechanism of Epimedium herb (EH) on rheumatoid arthritis (RA) treatment. We employed network pharmacology, molecular docking, and HPLC analysis to investigate the molecular mechanisms underlying the efficacy of EH in treating RA. To assess the efficacy of EH intervention, RA fibroblast-like synoviocytes (RA-FLS) and collagen-induced arthritis (CIA) mouse models were utilized. Ultimately, the active compounds icariin, luteolin, quercetin, and kaempferol were identified, with interleukin-1 beta (IL-1 beta), IL-6, tumor necrosis factor-alpha (TNF-alpha), and matrix metalloproteinase-9 (MMP-9) emerging as key targets of EH for RA. These targets were found to be downregulated in both in vitro and in vivo experiments following EH intervention. Furthermore, EH treatment induced apoptosis, reduced metastasis and invasion in RA-FLS, and ameliorated arthritis-related symptoms while regulating Th17 and Treg cells in CIA mice.
引用
收藏
页数:21
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