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.
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.
Authors: Umesh K Shandilya; Kristen Lamers; Yashi Zheng; Nicole Moran; Niel A Karrow Journal: In Vitro Cell Dev Biol Anim Date: 2022-05-02 Impact factor: 2.416
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Authors: Chike Godwin Azike; Paul Abrahams Charpentier; Jirui Hou; Hua Pei; Edmund Man King Lui Journal: Chin Med Date: 2011-05-27 Impact factor: 5.455