The aim of this study was to examine the anabolic and anticatabolic functions of bavachin in primary rat chondrocytes. With bavachin treatment, chondrocytes survived for 21 d without cell proliferation, and the proteoglycan content and extracellular matrix increased. Short-term monolayer culture of chondrocytes showed that gene induction of both aggrecan and collagen type II, major extracellular matrix components, was significantly upregulated by bavachin. The expression and activities of cartilage-degrading enzymes such as matrix metalloproteinases and a disintegrin and metalloproteinase with thrombospondin motifs were inhibited significantly by bavachin, while tissue inhibitors of metalloprotease were significantly upregulated. Bavachin inhibits the expression of inducible nitric oxide synthase, a representative catabolic factor, and downregulated the expression of nitric oxide, cyclooxygenase-2, and prostaglandin E 2 in a dose-dependent manner in chondrocytes. Our results suggest that the bavachin has anabolic and potent anticatabolic biological effects on chondrocytes, which may have considerable promise in treating articular cartilage degeneration in the future.Key words Osteoarthritis (OA); articular cartilage; chondrocyte; phytoestrogen; bavachin Osteoarthritis (OA) is a representative degenerative disease associated with aging and is the most common type of arthritis.1) The clinical symptoms of OA are defined as chronic joint pain, stiffness, and loss of mechanical joint function caused by progressive cartilage degeneration.2) Moreover, the prevalence of OA is largely age-dependent and is increased significantly in people over age 65.1) Although the prevalence of OA is less in those under 40, prevalence is increasing in these populations because of obesity, individual heredity, mechanical injuries, and surgical trauma of joints.1) The socioeconomic burden associated with OA is increased by both direct medical expenses and indirect costs caused by decreased productivity in the workplace.2) Although various studies on the pathophysiological etiologies of OA are ongoing, many of the factors causing this disease are still unknown. Hence, clinical treatments of OA have been mainly focused on relieving chronic joint pain by suppressing inflammation in the degenerative joint more so than on cartilage regeneration.Homeostasis of articular cartilage is precisely regulated by the balance between synthesis (anabolism) and degradation (catabolism) of the extracellular matrix (ECM), which is mainly composed of collagen Type II and proteoglycan synthesized from chondrocytes to maintain mechanical function in response to a compressive overload on joints.3) However, perturbations in chondrocytes with normal metabolic properties induce the progressive destruction of ECM through the up-regulation of cartilage-degrading enzymes such as matrix metalloproteinase (MMP)-13, MMP-3, MMP-1, a disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS)-4 and ADAMTS-5.3) Recent research has focused on cartilage regenerati...