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Int Immunopharmacol. 2007 Oct;7(10):1286-91. Epub 2007 Jun 26.

Anti-arthritic effect of ginsenoside Rb1 on collagen induced arthritis in mice.

Author information

1
Department of Internal Medicine, Hallym University Sacred Heart Hospital, Anyang, Republic of Korea. kimha@hallym.ac.kr

Abstract

BACKGROUND:

The development of orally bioavailable, inexpensive inhibitors of tumor necrosis factor (TNF)-alpha is desirable for the treatment of rheumatoid arthritis (RA).

OBJECTIVE:

To show the efficacy of ginsenoside Rb1 (G-Rb1), a ginseng extract, on the inhibition of TNF-alpha upregulation and on the inhibition of collagen induced arthritis (CIA).

METHODS:

Peripheral blood mononuclear cells (PBMC), chondrocytes and fibroblast-like synoviocytes (FLS) were stimulated with interferon(IFN)-gamma, lipopolysaccharide (LPS) or interleukin-1 in the presence or absence of G-Rb1. The concentrations of (TNF)-alpha in the culture supernatants were determined by ELISA. CIA was induced in DBA/1J mice and G-Rb1 was prophylactically administered from day 20 until day 39 following immunization. Histopathologic changes were scored, and the expression of TNF-alpha was evaluated by immunohistochemistry.

RESULT:

G-Rb1 significantly inhibited TNF-alpha upregulation in PBMCs, FLS and chondrocytes induced by IFN-gamma, LPS or IL-1. Administration of G-Rb1 resulted in a significant amelioration of the clinical arthritis score in the CIA mice. Histology revealed that G-Rb1 reduced cell infiltration and cartilage destruction in the arthritic joint, which was accompanied by a significant decrease in TNF-alpha expression.

CONCLUSION:

The utilization of G-Rb1 is a feasible approach to the treatment of RA or other diseases characterized by upregulation of TNF-alpha.

PMID:
17673143
DOI:
10.1016/j.intimp.2007.05.006
[Indexed for MEDLINE]

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