Abstract
As a joint disease, osteoarthritis (OA) is caused by the breakdown of subchondral bone and cartilage damage. Inflammatory factors, such as interleukin- (IL-) 1β, mediate the progression of OA. Madecassoside (MA), a triterpenoid component derived from the gotu kola herb (Centella asiatica), exhibits various pharmacological effects, including antioxidative and anti-inflammatory properties. In the present study, the protective effects and possible mechanism of MA on the treatment of OA were investigated. MA was demonstrated to significantly suppress the IL-1β-induced overexpression of matrix metalloproteinase- (MMP-) 3, MMP-13, inducible nitric oxide synthase (iNOS), and cyclooxygenase-2 (COX-2) and to decrease the IL-1β-induced degradation of type II collagen and sox9. Additionally, MA was able to reduce the IL-1β-induced phosphorylation of p65 in osteoarthritic chondrocytes. Furthermore, in a rat OA model, MA prevented cartilage degeneration and reduced the OARSI score in the MA-treated group compared with the OA group. The present study showed that MA suppresses the nuclear factor-κB signaling pathway, reducing IL-1β-induced chondrocyte inflammation, which indicates the therapeutic potential of MA in patients with OA.
Highlights
Osteoarthritis (OA) is a musculoskeletal disorder in the aged population [1]
The present study showed that MA suppresses the nuclear factor-κB signaling pathway, reducing IL-1β-induced chondrocyte inflammation, which indicates the therapeutic potential of MA in patients with OA
prostaglandin E2 (PGE2) may increase matrix metalloproteinase- (MMP-)13 production, which leads to collagen degradation [8] and the IL-1β-induced suppression of the inflammatory response may suppress the development of OA
Summary
Osteoarthritis (OA) is a musculoskeletal disorder in the aged population [1]. OA is the most common cause of disability among aging patients in the US [2]; it is characterized by a gradual loss of articular cartilage, joint stiffness, and chronic pain and severely affects quality of life. A number of factors, such as sex, weight, and trauma, may increase the risk of developing OA [3], which may result in joint degeneration. Previous studies showed the impact of inflammatory mediators on the pathological mechanism of OA. Among these inflammatory mediators, interleukin(IL-) 1β has been recognized as an important instigator of the pathophysiological development of OA [5]. It is able to stimulate chondrocyte-induced activation of the nuclear factor- (NF-) κB pathway, resulting in the upregulation of cartilage degrading enzymes such as matrix metalloproteinase- (MMP-) 1, MMP-3, and MMP-13 [6, 7]. PGE2 may increase MMP-13 production, which leads to collagen degradation [8] and the IL-1β-induced suppression of the inflammatory response may suppress the development of OA. The presented study is aimed at investigating the protective role of MA on IL1β-induced osteoarthritic chondrocytes, in addition to its underlying mechanism
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