Acteoside Counteracts Interleukin-1?-Induced Catabolic Processes through the Modulation of Mitogen-Activated Protein Kinases and the NF?B Cellular Signaling Pathway

Osteoarthritis (OA) is the most common degenerative joint disease with chronic pain caused by progressive degeneration of articular cartilage at synovial joints. Acteoside, a caffeoylphenylethanoid glycoside, has various biological activities such as antimicrobial, anti-inflammatory, anticancer, antioxidative, cytoprotective, and neuroprotective effect. Further, oral administration acteoside high dosage does not cause genotoxicity. Therefore, aim present study to verify anticatabolic effects against osteoarthritis its signaling pathway. Acteoside did decrease viabilities mouse fibroblast L929 cells used normal primary rat chondrocytes. counteracted IL-1?-induced proteoglycan loss in chondrocytes through suppressing expression activation cartilage-degrading enzyme matrix metalloproteinase- (MMP-) 13, MMP-1, MMP-3. Furthermore, suppressed inflammatory mediators inducible nitric oxide synthase, cyclooxygenase-2, oxide, prostaglandin E2 treated IL-1?. Subsequently, proinflammatory cytokines was decreased Moreover, only phosphorylation mitogen-activated protein kinases IL-1? but also translocation NF?B from cytosol nucleus suppression phosphorylation. Oral 5 10 mg/kg attenuated osteoarthritic model generated destabilization medial meniscus. Our findings indicate that promising potential agent or supplement attenuate prevent cartilage.