Polygonatum sibiricum polysaccharide inhibits IL-1β-induced inflammation in human chondrocytes

Jun Wu,Xinyu Zhang,Suohua Pan,Suqin Hu,Cunliang Wang

doi:10.1590/fst.44021

Abstract

Osteoarthritis (OA) is a degenerative joint disease associated with inflammation. Polygonatum sibiricum polysaccharide (PSP) is a major group of active components isolated from Polygonatum sibiricum with broad activities including anti-inflammatory effect. However, the role of PSP in OA is unclear. In the present study, we aimed to investigate the effects of PSP on IL-1β-induced inflammatory response in primary human OA chondrocytes. The results showed that PSP improved cell viability of chondrocytes in response to IL-1β induction. The increased levels of several inflammatory mediators including nitric oxide (NO), prostaglandin E2 (PGE2), inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) in IL-1β-induced chondrocytes were attenuated by PSP in a dose-dependent manner. The IL-1β-induced production of pro-inflammatory cytokines, TNF-α and IL-6, were mitigated by PSP in chondrocytes. Besides, PSP also suppressed the production of matrix metalloproteinases (MMPs), including MMP-1, MMP-3 and MMP-13 in IL-1β-stimulated chondrocytes. Furthermore, the IL-1β-induced activation of NF-κB signaling pathway in chondrocytes was also prevented by PSP. These findings suggested that PSP alleviated IL-1β-induced inflammatory response in chondrocytes via inhibiting NF-κB signaling pathway.

Highlights

Osteoarthritis (OA) is a degenerative joint disease and leading cause of morbidity and physical limitation among the elderly population (Loeser et al, 2012)
We examined the cytotoxic effect of Polygonatum sibiricum polysaccharide (PSP) on chondrocytes, chondrocytes were treated with various concentrations of PSP (0, 6.25, 12.5, 25 and 50 μM) for 24 h
The results showed that the highest concentration of PSP (50 μM) decreased chondrocyte viability, while PSP at concentrations of 0-25 μM was not cytotoxic to chondrocytes (Figure 1A)

Summary

Introduction

Osteoarthritis (OA) is a degenerative joint disease and leading cause of morbidity and physical limitation among the elderly population (Loeser et al, 2012). Pathological examinations show that OA is characterized by articular cartilage degradation, subchondral bone sclerosis, osteophyte formation, and inflammation (Malemud, 2015; Shen et al, 2017). Growing number of studies prove that inflammatory response plays crucial roles in the development of OA (Marchev et al, 2017; Shen et al, 2017). Upregulation of inflammatory mediators has been observed in synovial cells, articular chondrocytes and other cell types of diarthrodial cartilage (Rahmati et al, 2016). The inflammatory mediators lead to the degradation of cartilage extracellular matrix (ECM) via regulating the expressions of matrix metalloproteinases (MMPs) and a disintegrin and metalloproteinase with thrombospondin motifs (ADAMTSs) (Scanzello, 2017). It has been proposed that targeting the inflammation might be a promising strategy for the treatment of OA (Shen et al, 2017)

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