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Effect of Alpinia galanga extract on cartilage degradation and on gene expression in human chondrocyte and synovial fibroblast metabolism

We investigated the effects of A. galanga extract on metabolism and gene expression involved in the interleukin-1β (IL-1β) response of human chondrocyte and synovial fibroblast. A. galanga extract inhibited IL-1β enhanced matrix breakdown of the cartilage explants in a dose-dependent manner. It supp...

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Bibliographic Details
Published in:Central European journal of biology 2006-09, Vol.1 (3), p.430-450
Main Authors: Pothacharoen, Peraphan, Choocheep, Kanyamas, Pitak, Tanyaluck, Pompimon, Wilart, Premanode, Bhusana, Hardingham, Timothy, Kongtawelert, Prachya
Format: Article
Language:English
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Summary:We investigated the effects of A. galanga extract on metabolism and gene expression involved in the interleukin-1β (IL-1β) response of human chondrocyte and synovial fibroblast. A. galanga extract inhibited IL-1β enhanced matrix breakdown of the cartilage explants in a dose-dependent manner. It suppressed uronic acid loss from the tissue and decreased the release of sulfated GAG and hyaluronan into the medium. MMP-2 and MMP-9 activity in the culture medium of chondrosarcomas and synovial fibroblasts were significantly reduced in the presence of A. galanga extract, which also suppressed the production of MMP-1,-3 and-13. The A. galanga extract also significantly increased type II collagen, SOX9 and aggrecan gene expression, suggesting an ability to enhance anabolic activity. At a high dose of A. galanga extract there was a down-regulation of aggrecan gene expression. Comparison with Diacerein® showed its general anti-inflammatory potential to be similar. The A. galanga extract was shown to inhibit IL-1β-stimulated cartilage matrix degradation in both systems. Additionally, the extract showed the potential to up-regulate certain chondrocyte anabolic genes. It may, therefore, offer some cartilage protective and anti-inflammatory properties as a therapeutic agent in arthritis.
ISSN:2391-5412
1895-104X
2391-5412
1644-3635
DOI:10.2478/s11535-006-0030-6