Curcumin (CUR) is used in treating knee osteoarthritis (KOA), but its effects on synovial fibrosis and underlying mechanisms remain unclear. In vivo, a rat KOA model was established via anterior cruciate ligament transection (ACLT), followed by CUR administration. Synovial fibrosis, autophagy, and PI3K/AKT/mTOR pathway were assessed. In vitro, TGF-β1-induced fibroblast-like synoviocytes (FLSs) were treated with CUR. Fibrosis markers, autophagy activity, and PI3K/AKT/mTOR pathway proteins were analyzed. CUR alleviated synovial fibrosis in ACLT-induced rats. In FLSs, CUR reduced TGF-β1-stimulated fibrosis, suppressed PI3K/Akt/mTOR signaling, and enhanced autophagy. In vivo results confirmed CUR inhibited PI3K/Akt/mTOR and activated autophagy. CUR attenuated synovial fibrosis by activating protective autophagy via inhibition of the PI3K/Akt/mTOR pathway, elucidating a novel anti-fibrotic mechanism for KOA therapy.
He et al. (Mon,) studied this question.