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J Rheum Dis. 2015 Jun;22(3):154-166. English. Original Article.
Lee YJ , Song KY , Lee EY , Kang HS , Song YW .
Department of Internal Medicine, Seoul National University Bundang Hospital, Seongnam, Korea.
Department of Internal Medicine, Seoul National University College of Medicine, Seoul, Korea.
Department of Dermatology and Histopathology, College of Medicine, Chung-Ang University, Seoul, Korea.
Department of Internal Medicine, Seoul National University Hospital, Seoul, Korea.
Metabolab Inc., Cancer Research Institute, Seoul National University College of Medicine, Seoul, Korea.
Department of Molecular Medicine and Biopharmaceutical Sciences, Graduate School of Convergence Science and Technology, Medical Research Center, Seoul National University, Seoul, Korea.

OBJECTIVE: Although several ginsenosides have been reported to have anti-arthritic activity, few in vivo studies of the anti-arthritic effects of compound K (CK), a major metabolite of ginsenosides, have been conducted. Therefore, we investigated the preventative and therapeutic effects of CK on collagen-induced arthritis (CIA). METHODS: CK was administered to CIA mice preventively and therapeutically and post-treatment bone microarchitectural characteristics, histopathological changes, and serum levels of anti-collagen antibodies, tumor necrosis factor-alpha, and interleukin (IL)-17 were investigated. We also examined cytokine production by type II collagen (CII)-stimulated splenocytes and mRNA expression of matrix metalloproteinases (MMPs), tissue inhibitors of metalloproteinase (TIMP)-1, receptor activator of nuclear factor-kappaB ligand (RANKL), and osteoprotegerin (OPG) in the joint tissues. RESULTS: CK reduced the severity of CIA preventively and therapeutically (all p<0.05). Additionally, CK dose-dependently decreased histopathological signs of arthritis and improved microarchitectural characteristics (all p<0.05) at 10 to 20 mg/kg/d in CIA mice. CK treatment significantly decreased the serum levels of anti-CII immunoglobulin G (p<0.01) and the secretion of interferon-gamma and IL-2 from stimulated splenocytes (all p<0.05). Furthermore, MMP-3/TIMP-1 and RANKL/OPG ratios were suppressed in CK treated mice (all p<0.01). CONCLUSION: CK attenuated CIA via suppression of the humoral immune response and modulation of joint-destructive mediators. These results suggest that CK has therapeutic potential in rheumatoid arthritis.

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