title: β-Ecdysterone suppresses interleukin-1β-induced apoptosis and inflammation in rat chondrocytes via inhibition of NF-κB signaling pathway.
abstract: Osteoarthritis (OA) is characterized by a loss of articular cartilage accompanied with inflammation of synovium. β-Ecdysterone (Ecd), a major component of several Chinese herbal medicines, e.g., Achyranthes bidentata BL., has been used for the prevention and treatment of OA. Ecd is an estrogen analog and is likely to have similar pharmacological effects including the effect of protective chondrocytes. This study investigated the effects of Ecd on interleukin-1β (IL-1β)-induced apoptosis and inflammation in rat chondrocytes. Ecd protected chondrocytes from IL-1β-induced injury by inhibiting expression of Bax, p53 phosphorylation, and promoting expression of Bcl-xL . Simultaneously, Ecd reduced caspase 3 activity. IL-1β-induced inflammation and matrix degration were also prevented by Ecd via down-regulation of matrix metalloproteinases MMP 3, MMP 9, and cyclooxygenase-2 expression. Additionally, Ecd inhibited Nuclear Factor Kappa B (NF-κB) p65 phosphorylation, IκBα degradation, and phosphorylation in IL-1β-induced rat chondrocytes. These results suggested Ecd exerted anti-apoptosis and anti-inflammation in IL-1β-induced rat chondrocytes, which might be related to NF-κB signal pathway.
authors.affiliation: School of Biomedical Science, Huaqiao University, Quanzhou, China.
authors.forename: Xiaohong
authors.initials: X
authors.lastname: Zhang
authors.forename: Xianxiang
authors.initials: X
authors.lastname: Xu
authors.forename: Tao
authors.initials: T
authors.lastname: Xu
authors.forename: Si
authors.initials: S
authors.lastname: Qin
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D017209:Apoptosis / Q000187:drug effects*; D051017:Apoptosis Regulatory Proteins / Q000378:metabolism; D002470:Cell Survival / Q000187:drug effects; D002478:Cells, Cultured; D019902:Chondrocytes / Q000187:drug effects* / Q000378:metabolism; D004441:Ecdysterone / Q000494:pharmacology*; D020672:I-kappa B Proteins / Q000378:metabolism; D007249:Inflammation / Q000378:metabolism; D053583:Interleukin-1beta / Q000494:pharmacology*; D008297:Male; D019278:Matrix Metalloproteinase 3 / Q000378:metabolism; D020780:Matrix Metalloproteinase 9 / Q000378:metabolism; D000072000:NF-KappaB Inhibitor alpha; D017207:Rats, Sprague-Dawley; D015398:Signal Transduction / Q000187:drug effects; D051996:Transcription Factor RelA / Q000378:metabolism*; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism
chemical_list: D000893:Anti-Inflammatory Agents; D051017:Apoptosis Regulatory Proteins; D020672:I-kappa B Proteins; D053583:Interleukin-1beta; C000606206:Nfkbia protein, rat; D051996:Transcription Factor RelA; D016159:Tumor Suppressor Protein p53; D000072000:NF-KappaB Inhibitor alpha; D004441:Ecdysterone; D019278:Matrix Metalloproteinase 3; D020780:Matrix Metalloproteinase 9; C572337:Mmp9 protein, rat
keywords: NF-κB; apoptosis; chondrocytes; inflammation; β-Ecdysterone