International immunopharmacology · 2007
Anti-arthritic effect of ginsenoside Rb1 on collagen induced arthritis in mice.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Kim Hyun Ah, Kim Suho, Chang Sun Hwa, Hwang Hea Jun, Choi Young-nim
Аннотация
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.
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.