Abstract
Osteoarthritis (OA) is the most common degenerative joint disease with chronic joint 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 of acteoside at high dosage does not cause genotoxicity. Therefore, the aim of present study is to verify the anticatabolic effects of acteoside against osteoarthritis and its anticatabolic signaling pathway. Acteoside did not decrease the viabilities of mouse fibroblast L929 cells used as normal cells and primary rat chondrocytes. Acteoside counteracted the IL-1β-induced proteoglycan loss in the chondrocytes and articular cartilage through suppressing the expression and activation of cartilage-degrading enzyme such as matrix metalloproteinase- (MMP-) 13, MMP-1, and MMP-3. Furthermore, acteoside suppressed the expression of inflammatory mediators such as inducible nitric oxide synthase, cyclooxygenase-2, nitric oxide, and prostaglandin E2 in the primary rat chondrocytes treated with IL-1β. Subsequently, the expression of proinflammatory cytokines was decreased by acteoside in the primary rat chondrocytes treated with IL-1β. Moreover, acteoside suppressed not only the phosphorylation of mitogen-activated protein kinases in primary rat chondrocytes treated with IL-1β but also the translocation of NFκB from the cytosol to the nucleus through suppression of its phosphorylation. Oral administration of 5 and 10 mg/kg acteoside attenuated the progressive degeneration of articular cartilage in the osteoarthritic mouse model generated by destabilization of the medial meniscus. Our findings indicate that acteoside is a promising potential anticatabolic agent or supplement to attenuate or prevent progressive degeneration of articular cartilage.
Highlights
Osteoarthritis (OA) is the most common degenerative joint disease with chronic joint pain caused by progressive degeneration of articular cartilage at synovial joints [1].Due to the increase in life expectancy, the prevalence of OA with loss of mobility and chronic joint pain caused by progressive degeneration of articular cartilage at synovial joints is estimated to be 18% and 9.6% in women after menopause and in men, respectively [2]
Acteoside suppressed the expression of inflammatory mediators such as inducible nitric oxide synthase, cyclooxygenase-2, nitric oxide, and prostaglandin E2 in the primary rat chondrocytes treated with IL-1β
The number of dead cells stained as red fluorescence did not increase for both L929 cells and primary rat chondrocytes treated with 50 and 100 μM acteoside for 24 h
Summary
Osteoarthritis (OA) is the most common degenerative joint disease with chronic joint pain caused by progressive degeneration of articular cartilage at synovial joints [1]. Due to the increase in life expectancy, the prevalence of OA with loss of mobility and chronic joint pain caused by progressive degeneration of articular cartilage at synovial joints is estimated to be 18% and 9.6% in women after menopause and in men, respectively [2]. The Oxidative Medicine and Cellular Longevity worldwide prevalence of OA increases annually, the pathophysiological etiology of OA is still unknown. It may be caused by very complex and multifactorial risk factors such as aging, gender, genetic inheritance, traumatic joint injury, and severe mechanical joint load. The demand for development of effective intervention or supplementation, with long-term biological safety, to prevent or attenuate OA to maintain life quality through maintenance of mechanical joint function in the elderly population is increasing
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