Abstract
Osteoarthritis (OA) is an age-related degenerative disease that causes cartilage dysfunction and inflammation. Obtusifolin, an anthraquinone extracted from Senna obtusifolia (L.) H.S.Irwin & Barneby seeds, has anti-inflammatory functions; it could be used as a drug component to relieve OA symptoms. In this study, we investigated the effects of obtusifolin on OA inflammation. In vitro, interleukin (IL)-1β (1 ng/mL)-treated mouse chondrocytes were co-treated with obtusifolin at different concentrations. The expression of matrix metalloproteinase (Mmp) 3, Mmp13, cyclooxygenase 2 (Cox2), and signaling proteins was measured by polymerase chain reaction and Western blotting; collagenase activity and the PGE2 level were also determined. In vivo, OA-induced C57BL/6 mice were administered obtusifolin, and their cartilage was stained with Safranin O to observe damage. Obtusifolin inhibited Mmp3, Mmp13, and Cox2 expression to levels similar to or more than those after treatment with celecoxib. Additionally, obtusifolin decreased collagenase activity and the PGE2 level. Furthermore, obtusifolin regulated OA via the NF-κB signaling pathway. In surgically induced OA mouse models, the cartilage destruction decreased when obtusifolin was administered orally. Taken together, our results show that obtusifolin effectively reduces cartilage damage via the regulation of MMPs and Cox2 expression. Hence, we suggest that obtusifolin could be a component of another OA symptom reliever.
Highlights
The molecules involved in cartilage destruction and inflammation include matrix metalloproteinases (MMPs) and cyclooxygenase 2 (Cox2), which are catabolic factors [3,4]
Treatment at the indithe indicated concentrations for 24 h did not reduce the viability of chondrocytes (Figure cated concentrations for 24 h did not reduce the viability of chondrocytes (Figure 1B)
Summary of Mechanism treated with obtusifolin at the indicated concentrations for 24 h, and IL-1β (1 ng/mL) was added 10 min before harvest
Summary
Osteoarthritis (OA) is a degenerative disease caused by cartilage destruction or joint cartilage inflammation and usually occurs in elderly individuals [1,2]. The molecules involved in cartilage destruction and inflammation include matrix metalloproteinases (MMPs) and cyclooxygenase 2 (Cox2), which are catabolic factors [3,4]. The expression of these factors is increased by proinflammatory cytokines (interleukin (IL)-1β, tumor necrosis factor-α, and IL-17) [5,6]. Among the MMPs, Mmp and Mmp degrade the extracellular matrix by inducing aggrecanase and collagenase activities and increasing the PGE2 level, causing cartilage degradation and, thereby, resulting in OA [5,7].
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