Currently, osteoarthritis as degenerative chronic joint disease remains unsolved and finding the effective targeting therapeutic agent is pressing. Therefore, in this research, we aimed to investigate the effects of cardamonin, the NF-kb inhibitor, in cell model of osteoarthritis. IL-1β
that induced chondrocytes served as the cell model of osteoarthritis. The cells were divided into control, IL-1β and IL-1+ cardamonin groups. Western blot assays were performed for assessment of protein expression level and PCR for gene level. Flow cytometry was used for cell
apoptosis detection. MDA, LDH SOD and ROS were detected by corresponding kits. The NF-kb was activated by IL-1. The entrance of NF-kb into cell nucleus was inhibited by cardamonin in IL-1β-induced cells. The MDA, LDH and ROS were increased by IL-1β and SOD was down-regulated by IL-1β.
This effect of IL-1β was reduced by cardamonin. The cell apoptosis and pro-apoptosis proteins were increased and BCl-2 was down-regulated in IL-1β-induced cells. After cardamonin treatment, this effect was inhibited. The extracellular matrix degradation as well as the relative degradation
enzymes was elevated by IL-1β, and this effect was further inhibited by cardamonin as well. Cardamonin exerted protective effects via alleviating oxidative stress, cell apoptosis level and extracellular matrix degradation by inhibiting NF-kb in IL-1β-induced chondrocytes. Cardamonin
as NF-kb inhibitor was a promising drug for therapy of osteoarthritis.
Bardoxolone-Methyl Prevents Oxidative Stress-Mediated Apoptosis and Extracellular Matrix Degradation in vitro and Alleviates Osteoarthritis in vivo
