Дорно дахины уламжлалт анагаах ухаан, 2012, 2(3)
THERAPEUTIC EFFICACY OF SUNLAVIN, AN ARTHRITIS RELIEF TEA ON ANTIGEN-INDUCED ARTHRITIS IN RABBITS
( Тойм өгүүлэл )
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Абстракт
Introduction: Rheumatoid arthritis (RA) is a chronic and systemic inflammatory
disorder affecting multiple joints. Although etiology of RA is not fully understood,
TNF-alpha has been shown to play a central role in the pathogenesis of RA. TNF-alpha
stimulates proliferation of synovial cells and the production of matrix
metalloproteinases by chondrocytes and synovial cells, and induces the release of other
pro-inflammatory cytokines, leading to joint destruction.
Objectives: The aim of the present study was to investigate the therapeutic effects of
sunlavin, an arthritis relief tea on antigen-induced arthritis in rabbits.
Methods: Arthritis of the knee joints was induced by ovalbumin injection into the joint
spaces of pre-immunised rabbits. For time course experiments sunlavin was
administered to rabbits for 7, 20, 34, and 49 days. Histopathological analysis of the
synovial tissue was performed. Level of tumor necrosis factor-alpha (TNF-alpha),
erythrocyte sedimentation rate (ESR), C reactive protein (CRP) level, and white blood
cells count (WBC) were measured.
Results: Sunlavin reduced joint swelling of antigen-induced arthritis model of rabbits.
Histological examination revealed that sunlavin reduced edematous changes and
infiltration of inflammatory cells in the synovial tissues. Increases in ESR, CRP, and
WBC were reduced up to 52% by sunlavin. Moreover, sunlavin decreased blood level
of TNF-alpha (21%) in rabbit model of antigen-induced arthritis suggesting that
sunlavin ameliorates inflammatory response in arthritic joints by inhibiting THF-alpha.
Discussions and conclusions: We speculate that the effect of sunlavin might be
affected by the tissue environment and the disease state, that is, the effect of sunlavin
on inflammation may change during the inflammatory process.
Sunlavin can be a potential anti-inflammatory agent for acute and chronic phase of
inflammation.
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