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-1β 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-κB signaling pathway, Schisandrol A suppressed the degradation of IκB and the phosphorylation of p65 induced by IL-1β. Overall, and Schisandrol A reduced the expression of catabolic factors by blocking NF-κB signaling and prevented cartilage destruction. Therefore, Schisandrol A attenuated OA progression, and can be used to develop novel OA drug therapies.
Highlights
Joint inflammation and cartilage destruction are the leading causes of osteoarthritis (OA) and are responsible for making a patient’s daily life uncomfortable [1]
The molecular mechanisms of inflammation and cartilage destruction are driven by the induction of catabolic factors such as matrix metalloproteinases (MMPs), aggrecanase, and cyclooxygenase 2 (COX-2) [8]
We examined whether Schisandrol A is toxic to chondrocytes
Summary
Joint inflammation and cartilage destruction are the leading causes of osteoarthritis (OA) and are responsible for making a patient’s daily life uncomfortable [1]. OA has several risk factors such as aging, gender, obesity, and reactive oxygen species (ROS) production, which influence a variety of processes and lead to joint destruction. Such factors increase susceptibility to cell death leading to defect repair of the damaged matrix and inflammatory and catabolic conditions, in turn, promoting the development of OA by imbalance in joints [4,5,6].
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