Abstract
BackgroundOsteoarthritis (OA) is characterized by inflammation and extracellular matrix (ECM) degradation and is one of the most common chronic degenerative joint diseases that causes pain and disability in adults. Urolithin A (UA) has been widely reported for its anti-inflammatory properties in several chronic diseases. However, the effects of UA on OA remain unclear. The aim of the current study was to investigate the anti-inflammatory effects and mechanism of UA in interleukin-1β (IL-1β)-induced chondrocytes.ResultsNo marked UA cytotoxicity was noted, and UA protected cartilage from damage following IL-1β stimulation in micromasses. Moreover, UA promoted the expression of anabolic factors including Sox-9, Collagen II, and Aggrecan while inhibiting the expression of catabolic factors such as matrix metalloproteinases (MMPs) and a disintegrin and metalloproteinase with thrombospondin motifs 4 (ADAMTS-4) in rat chondrocytes. Protective effects of UA were also observed in ex vivo organ culture of articular cartilage. Mechanistically, IL-1β significantly activated and upregulated the expression of p-ERK 1/2, p-JNK, p-P38, and p-P65, while UA protected chondrocytes against IL-1β-induced injury by activating the mitogen-activated kinase (MAPK)/nuclear factor-κB (NF-κB) signaling pathways.ConclusionOur results provide the evidence that UA could attenuate IL-1β-induced cell injury in chondrocytes via its anti-inflammatory action. UA may be a promising therapeutic agent in the treatment of OA.
Highlights
Osteoarthritis (OA) is one of the most common forms of chronic degenerative joint disease and affects tens of millions of people around the world [1]
We investigated the anti-inflammatory role of Urolithin A (UA) by attenuating IL-1β-induced degradation of Collagen Type II collagen (II) and Aggrecan and by reducing the production of inflammatory mediators via the ERK, JNK, P38, and nuclear factor-κB (NF-κB) pathways in rat chondrocytes
Cell viability after IL-1β or/and UA treatment First, we examined the potential toxicity of UA on chondrocytes with CCK8 assays
Summary
Osteoarthritis (OA) is one of the most common forms of chronic degenerative joint disease and affects tens of millions of people around the world [1]. A growing body of evidence suggests that interleukin-1β (IL-1β), tumor necrosis factor-alpha (TNF-α), and IL-6 are found in OA cartilage [6]. Among these inflammatory cytokines, the effect of IL-1β was widely explored because of its vital role in inflammatory responses. Osteoarthritis (OA) is characterized by inflammation and extracellular matrix (ECM) degradation and is one of the most common chronic degenerative joint diseases that causes pain and disability in adults. Urolithin A (UA) has been widely reported for its anti-inflammatory properties in several chronic diseases. The aim of the current study was to investigate the anti-inflammatory effects and mechanism of UA in interleukin-1β (IL-1β)-induced chondrocytes
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