Compound K, a Metabolite of Ginsenosides, Attenuates Collagen-induced Arthritis in Mice.
10.4078/jrd.2015.22.3.154
- Author:
Yun Jong LEE
1
;
Kye Yong SONG
;
Eun Young LEE
;
Heun Soo KANG
;
Yeong Wook SONG
Author Information
1. Department of Internal Medicine, Seoul National University Bundang Hospital, Seongnam, Korea.
- Publication Type:Original Article
- Keywords:
Panax;
Ginsenoside M1;
Experimental arthritis;
Rheumatoid arthritis
- MeSH:
Animals;
Antibodies, Neoplasm;
Arthritis;
Arthritis, Experimental*;
Arthritis, Rheumatoid;
Collagen Type II;
Ginsenosides*;
Immunity, Humoral;
Immunoglobulin G;
Interferon-gamma;
Interleukin-2;
Interleukins;
Joints;
Matrix Metalloproteinases;
Mice*;
Necrosis;
Osteoprotegerin;
Panax;
RANK Ligand;
RNA, Messenger
- From:Journal of Rheumatic Diseases
2015;22(3):154-166
- CountryRepublic of Korea
- Language:English
-
Abstract:
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.
