Cordycepin prevented IL-β-induced expression of inflammatory mediators in human osteoarthritis chondrocytes

Abstract

Purpose Cordycepin, a nucleoside derivative isolated from Cordyceps, has been reported to exert anti-inflammatory, antitumor, antidiabetic and renoprotective effects. Osteoarthritis (OA) is a degenerative joint disease with an inflammatory component that drives the degradation of cartilage extracellular matrix. This study aimed to assess the effects of cordycepin on human OA chondrocytes. Methods In this study, human OA chondrocytes were pretreated with cordycepin at 10, 50 or 100 μM and subsequently stimulated with interleukin-1β (IL-1β) (5 ng/ml) for 24 h. Production of prostaglandin E 2 (PGE2) and nitric oxide (NO) were evaluated by the Griess reaction and an enzymelinked immunosorbent assay (ELISA). Gene expression of matrix metalloproteinase (MMP)-13, IL-6, inducible nitric oxide synthase (iNOS) and cyclo-oxygenase (COX-2) was measured by real-time polymerase chain reaction (PCR). MMP-13 and IL-6 proteins in culture medium were determined using cytokine-specific ELISA. Western immunoblotting was used to analyse the iNOS and COX-2 protein production in culture medium. Nuclear factor kappa-B (NF-κB) activity regulation was explored using Western immunoblotting. Results Pretreatment with cordycepin significantly inhibited the production of PGE2 and NO induced by IL-1β. Cordycepin also significantly decreased the IL-1β-stimulated gene expression and production of MMP-13, IL-6, iNOS and COX-2 in OA chondrocytes. Pretreatment with cordycepin attenuated IL-1β-induced activation of NF-κB by suppressing degradation of its inhibitory protein nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, alpha (IκB-α) in the cytoplasm. Conclusions We show for the first time the anti-inflammatory activity of cordycepin in human OA chondrocytes. Thus, with this unique profile of actions, cordycepin may prove to be a potentially attractive and new therapeutic/preventive agent for OA.

Astragalin inhibits IL-1β-induced inflammatory mediators production in human osteoarthritis chondrocyte by inhibiting NF-κB and MAPK activation

“…These inflammatory mediators are implicated in bone resorption and joint pain [23]. Accumulating evidence suggests that inhibition of these inflammatory mediators has therapeutic potential in the treatment of OA [8,24]. In this study, our results showed that astragalin inhibited IL-1β-induced NO and PGE2 production, as well as iNOS and COX-2 expression in chondrocytes.…”

“…Overproduction of NO and PGE2 leads to clinical manifestations [7]. Accumulating evidence suggests that neutralization of IL-1β-induced inflammatory mediators appears to be useful in the treatment of OA [8,9].…”

Dual specificity phosphatase 1 has a protective role in osteoarthritis fibroblast-like synoviocytes via inhibition of the MAPK signaling pathway

“…It has been known that MAPK signaling pathway has a critical role in the regulation of inflammatory and catabolic mediators, such as COX-2 and MMP-13 (36,37). In OA, MMP-13 and COX-2 have a critical role in maintaining cartilage homeostasis (15,38). MMP-13 is involved in type II collagen cleavage, which contributes to the degradation of joint cartilage.…”

Asiatic Acid Attenuates Osteoarthritis by Regulating NF-κB Signaling Pathway in Chondrocytes

“…Recent years, there are more and more interests in natural products, such as avocado soybean unsaponi ables [16], cordycepin [8], piperine [9], astragalin [10], etc., extracted from herbs as alternatives because of their potential anti-arthritic effects. Evidences have shown the potential role of natural products in the treatment of OA by regulating IL-1β-induced in ammatory mediators [17] [18] [19]. Asiatic acid (AA), a pentacyclic triterpene isolated from various plants including Centella asiatica, has shown anti-in ammation effect in many in ammatory conditions.…”