Specnuezhenide Decreases Interleukin-1β-Induced Inflammation in Rat Chondrocytes and Reduces Joint Destruction in Osteoarthritic Rats.

Chiyuan Ma,An Liu,Linyan Wang,Jisheng Ran,Shigui Yan,Kai Xu,Wei Wang,Yute Yang,Haobo Wu,Xiaopeng Zhou,Lidong Wu

doi:10.3389/fphar.2018.00700

Chiyuan Ma, An Liu + Show 9 more

Open Access

https://doi.org/10.3389/fphar.2018.00700

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Abstract

As a chronic disease, osteoarthritis (OA) leads to the degradation of both cartilage and subchondral bone, its development being mediated by proinflammatory cytokines like interleukin-1β. In the present study, the anti-inflammatory effect of specnuezhenide (SPN) in OA and its underlying mechanism were studied in vitro and in vivo. The results showed that SPN decreases the expression of cartilage matrix-degrading enzymes and the activation of NF-κB and wnt/β-catenin signaling, and increases chondrocyte-specific gene expression in IL-1β-induced inflammation in chondrocytes. Furthermore, SPN treatment prevents the degeneration of both cartilage and subchondral bone in a rat model of OA. To the best of our knowledge, this study is the first to report that SPN decreases interleukin-1β-induced inflammation in rat chondrocytes by inhibiting the activation of the NF-κB and wnt/β-catenin pathways, and, thus, has therapeutic potential in the treatment of OA.

Highlights

Osteoarthritis is one of the most common degenerative joint diseases, which involves cartilage loss, synovial inflammation and chronic pain (Benito et al, 2005; Loeuille et al, 2005)
The expression of cartilage matrix-degrading enzymes, such as matrix metalloproteinase (MMP)-3 and MMP-9, did not show significant changes. These results indicate that SPN treatment does not significantly impact rat chondrocyte viability or gene expression
To understand the anti-inflammatory mechanism of SPN, we investigated its effects on the IL-1β-induced activation of nuclear factor-κB (NF-κB) and wnt/β-catenin signaling in rat chondrocytes in vitro, by Western blotting

Summary

Introduction

Osteoarthritis is one of the most common degenerative joint diseases, which involves cartilage loss, synovial inflammation and chronic pain (Benito et al, 2005; Loeuille et al, 2005). Genetic and environmental factors, including sex, obesity, and injuries, could increase the risk of developing OA (Blagojevic et al, 2010). These factors can repeatedly disrupt the joint microenvironment, leading to its degeneration. The smooth functioning of joints is ensured by cartilages at the articular surface, which rely on the tensile strength of matrix induced by chondrocytes (Chen et al, 2002). Chondrocytes take part in the synthesis and degradation of cartilage matrix, and an inflammatory microenvironment could damage this function of chondrocytes (Liu-Bryan and Terkeltaub, 2015)

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