Curcumin ameliorates H2O2-induced inflammatory response in chondrocytes by inducing autophagy activation

xlomafota13 shared this article with you from Inoreader Curcumin ameliorates H<sub>2</sub>O<sub>2</sub>-induced inflammatory response in chondrocytes by inducing autophagy activation Via Experimental and therapeutic medicine Exp Ther Med. 2022 Apr;23(4):272. doi: 10.3892/etm.2022.11198. Epub 2022 Feb 9. ABSTRACT Relapsing polychondritis (RP) is a clinical disease characterized by inflammation of cartilage tissue and chondrocytes. The principal curcuminoid curcumin is the most active component in turmeric and has been reported to have a chondroprotective effect, including anti-inflammatory activity, which is vitally important for mitigating RP symptoms and prognosis. However, the mechanisms underlying these actions have remained to be fully elucidated. In the present study, the chondroprotective mechanisms of curcumin on hydrogen peroxide (H2O2)-treated primary chondrocytes were examined in vitro. The viability of chondrocytes treated with H2O2 was significantly reduced in a dose- and time-dependent manner. Cotreatment of curcumin with H2O2 significantly decreased growth inhibition. It was observed that curcumin inhibited the expression levels of the inflammatory mediators interleukin (IL)-1β, IL-6 and inducible nitric oxide synthase and induced autophagy activation. Curcumin increased the protein levels of the autophagy marker beclin-1 and light chain 3-II and decreased the expression levels of P62 in H2O2-treated chondrocytes. The curcumin-induced anti-inflammatory effects were markedly abrogated by the autophagy inhibitor 3-methyladenine. In conclusion, the present study suggested that curcumin regulates inflammatory factors by activating autophagy in chondrocytes. The protective role of curcumin in chondrocytes was demonstrated, suggesting that it should be explored for the prophylactic treatment of RP in the clinic in the future. PMID:35251338 | PMC:PMC8892606 | DOI:10.3892/etm.2022.11198 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.