KMID : 1084220150220030154
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Journal of Rheumatic Diseases 2015 Volume.22 No. 3 p.154 ~ p.166
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Compound K, a Metabolite of Ginsenosides, Attenuates Collagen-induced Arthritis in Mice
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Lee Yun-Jong
Song Kye-Yong Lee Eun-Young Kang Heun-Soo Song Yeong-Wook
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Abstract
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Objective: Although several ginsenosides have been reported to have anti-arthritic activity, few in vivo studies of the anti-ar-thritic 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 pre-ventively and therapeutically and post-treatment bone microarchitectural characteristics, histopathological changes, and serum levels of anti-collagen antibodies, tumor necrosis factor-¥á, and interleukin (IL)-17 were investigated. We also examined cyto-kine 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-¥êB ligand (RANKL), and osteoprotegerin (OPG) in the joint tissues.
Results: CK reduced the severity of CIA preventively and therapeutically (all p£¼0.05). Additionally, CK dose-dependently decreased histopathological signs of arthritis and improved microarchitectural characteristics (all p£¼0.05) at 10 to 20 mg/kg/d in CIA mice. CK treatment significantly decreased the serum levels of anti-CII immunoglobulin G (p£¼0.01) and the secretion of interferon-¥ã and IL-2 from stimulated splenocytes (all p£¼0.05). Furthermore, MMP-3/TIMP-1 and RANKL/OPG ratios were suppressed in CK treated mice (all p£¼0.01).
Conclusion: CK attenuated CIA via suppression of the humoral immune response and modulation of joint-destructive mediators. These results suggest that CK has therapeutic po-tential in rheumatoid arthritis.
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KEYWORD
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Panax, Ginsenoside M1, Experimental arthritis, Rheumatoid arthritis
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