The principal findings of the present study were: (i) T2DM caused knee OA and oral supplementation with CAR at doses of 0.3 and 0.9 g/kg partially alleviated T2DM-induced OA by reducing cartilage surface erosion, matrix loss, and inflammation of the synovium; (ii) the FLSs showed increased responsiveness to IL-1β-induced inflammation under the high glucose condition; and (iii) CAR suppressed the inflammatory response in IL-1β-induced FLSs under the high glucose condition via the ROS/NF-κB pathway. This evidence concerns the gene NFKB1 and type 2 diabetes mellitus.