In the management of osteoarthritis, EA (0, 12.5, 25, and 50 μM, 24 h; 50 mg/kg/day) decreased the production of some inflammatory mediators (NO, prostaglandin E2—PGE2, IL-6, TNF-α, COX-2, inducible form of nitric oxide synthase—iNOS, NF-κB), while up-regulating the expression of collagen type II and aggrecan in IL-1β-induced human chondrocytes in a dose-dependent manner, and higher levels of IL-10 in rats with osteoarthritis induced by monosodium iodoacetate [57,58]. Here, ACAN is linked to osteoarthritis.