Year-end Sale % OFF 
Abstract
Osteoarthritis (OA) is a common joint disease in the elderly population. Its development has been reported to be associated with cartilage degradation and inflammatory responses. Schisandrin A, a bioactive lignin in Schisandra sphenanthera, has shown its anti-inflammatory potential in various inflammation diseases. However, the effects of Schisandrin A on OA remain to explore. In this study, rat chondrocytes were treated with IL-1β (10 ng/ml) with or without different concentrations of Schisandrin A for 24 h. Cell viability was evaluated by CCK-8 assay. Production of nitric oxide (NO) and prostaglandin E2 (PGE2) was measured by the Griess reaction and ELISA. The MAPK/NF-κB-related signaling molecules expression and the protein production of inducible nitric oxide synthase (iNOS), cyclooxygenase (Cox)-2, MMPs (MMP1, MMP3, MMP13), ADAMTS5, Collagen II, aggrecan, and Sox9 were detected by Western blot. Protein expression of Collagen II, aggrecan, and p65 nuclear translocation was evaluated by immunofluorescence. In vivo, intra-articular injection of 50 μM Schisandrin A or equal volume of vehicle was performed on rat OA models. Severity of cartilage damage was evaluated by HE and Safranin-O-Fast green staining. Our results revealed that Schisandrin A could suppress the IL-1β-induced production of NO and PGE2 in rat chondrocytes. Consistent with these findings, the upregulation of iNOS and Cox2 could also been decreased by Schisandrin A. Additionally, Schisandrin A could inhibit IL-1β-induced cartilage matrix catabolic enzymes including MMPs and ADAMTS5. Moreover, the IL-1β-induced downregulation of Collagen II, aggrecan, and Sox9 could be ameliorated by Schisandrin A. Mechanistically, Schisandrin A functioned by suppressing MAPK and NF-κB signal pathways. In vivo, Schisandrin A prevented cartilage damage in rat OA model. In conclusion, this study elucidates that Schisandrin A inhibits the IL-1β-induced inflammation and cartilage degradation via suppression of MAPK and NF-κB signal pathways, indicating its potential role in OA therapy.
Highlights
Osteoarthritis (OA) is a chronic joint disease characterized by cartilage degeneration and physical disability (Jeon et al, 2017)
CCK-8 assay was employed to verify the cytotoxic effects of Schisandrin A on chondrocytes
To verify whether Schisandrin A could inhibit the upregulation of nitric oxide (NO) and prostaglandin E2 (PGE2) induced by IL-1β, the Griess reagent was performed to detect the NO concentration and an ELISA kit was used to evaluate the PGE2 level
Summary
Osteoarthritis (OA) is a chronic joint disease characterized by cartilage degeneration and physical disability (Jeon et al, 2017). Hallmarks of OA include arthrodynia, osteophyte formation, and subchondral bone sclerosis (Glyn-Jones et al, 2015). Pervasive cartilage damage due to inflammation and imbalance between anabolic and catabolic factors in joint is essential to the progression of OA (Appleton, 2018). As an age-related disease, OA affects 240 million people globally with about 10% of men and 18% of women over 60 years old (Nelson, 2018). It is confirmed that OA has doubled in prevalence since the mid20th century (Wallace et al, 2017). Due to lack of effective treatment for OA, most patients need joint replacement, leaving behind huge social and economic burdens (Bellamy et al, 2006)
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
