Curcumin ameliorates experimentally induced knee osteoarthritis in rats <i>via</i> regulation of synovial inflammatory.

This study was designrd to investigate the effect of curcumin on chondrosynovitis in knee osteoarthritis (KOA) rat models and to explore its mechanism of action. The damage of knee cartilage tissue was detected by haematoxylin and eosin (HE) staining, toluidine blue, safranin O-fast green and a scoring system by Mankin were used to assess the histopathological features of cartilage. Chondrocytic cells of apoptosis was visualized by TUNEL staining; inflammatory cytokines (interleukin-6, interleukin-1beta (IL-1β) and tumor necrosis factor alpha (TNF-α)) in the synovial fluid were examined by ELISA; immunohistochemistry (IHC) was used to detect cartilage oligomeric matrix protein (COMP) and fibroblast activation protein (FAP) expression was determined to evaluate cartilage damage and fibrosis. In comparison to the control group, rats induced by MIA demonstrated joint cartilage injury, chondrocyte apoptosis (P<0.001), and synovial inflammation (P<0.0001). However, when compared to the model group, curcumin administration significantly ameliorated cartilage damage, as evidenced by a reduction in Mankin score (P<0.0001), chondrocyte apoptosis (P<0.01), and levels of inflammatory factors (P<0.0001). In conclusion: monosodium iodoacetate (MIA) induction was employed to establish a KOA rat model. Treatment with curcumin improved synovial inflammation, reduced chondrocyte apoptosis, and decreased cartilage destruction in KOA rats.