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β‐Ecdysterone Suppresses Interleukin‐1β‐Induced Apoptosis and Inflammation in Rat Chondrocytes via Inhibition of NF‐κB Signaling Pathway
Author(s) -
Zhang Xiaohong,
Xu Xianxiang,
Xu Tao,
Qin Si
Publication year - 2014
Publication title -
drug development research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.582
H-Index - 60
eISSN - 1098-2299
pISSN - 0272-4391
DOI - 10.1002/ddr.21170
Subject(s) - inflammation , phosphorylation , matrix metalloproteinase , apoptosis , nf κb , iκbα , chemistry , signal transduction , interleukin , microbiology and biotechnology , pharmacology , cancer research , endocrinology , medicine , biology , cytokine , biochemistry
Preclinical ResearchOsteoarthritis ( OA ) is characterized by a loss of articular cartilage accompanied with inflammation of synovium. β‐Ecdysterone ( Ecd ), a major component of several C hinese herbal medicines, e.g., A chyranthes 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 B ax, p 53 phosphorylation, and promoting expression of Bcl ‐x L . 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.