Schisandrol A Suppresses Catabolic Factor Expression by Blocking NF-kappa B Signaling in Osteoarthritis
- Authors
- Han, Seong Jae; Jun, Jimoon; Eyun, Seong-il; Lee, Choong-Gu; Jeon, Jimin; Pan, Cheol-Ho
- Issue Date
- Mar-2021
- Publisher
- MDPI
- Keywords
- Schisandrol A; cartilage destruction; osteoarthritis; NF-kappa B
- Citation
- PHARMACEUTICALS, v.14, no.3
- Journal Title
- PHARMACEUTICALS
- Volume
- 14
- Number
- 3
- URI
- https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/51787
- DOI
- 10.3390/ph14030241
- ISSN
- 1424-8247
1424-8247
- Abstract
- Schisandrol A possesses pharmacological properties and is used to treat various diseases; however, its effects on osteoarthritis (OA) progression remain unclear. Here, we investigated Schisandrol A as a potential therapeutic agent for OA. In vitro, Schisandrol A effects were confirmed based on the levels of expression of catabolic factors (MMPs, ADAMTS5, and Cox2) induced by IL-1 beta or Schisandrol A treatment in chondrocytes. In vivo, experimental OA in mice was induced using a destabilized medial meniscus (DMM) surgical model or oral gavage of Schisandrol A in a dose-dependent manner, and demonstrated using histological analysis. In vitro and in vivo analyses demonstrated that Schisandrol A inhibition attenuated osteoarthritic cartilage destruction via the regulation of Mmp3, Mmp13, Adamts5, and Cox2 expression. In the NF-kappa B signaling pathway, Schisandrol A suppressed the degradation of I kappa B and the phosphorylation of p65 induced by IL-1 beta. Overall, and Schisandrol A reduced the expression of catabolic factors by blocking NF-kappa B signaling and prevented cartilage destruction. Therefore, Schisandrol A attenuated OA progression, and can be used to develop novel OA drug therapies.
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Collections - College of Natural Sciences > Department of Life Science > 1. Journal Articles
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