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Effects of compounds from Kaempferia parviflora on nitric oxide, prostaglandin E₂ and tumor necrosis factor-alpha productions in RAW264.7 macrophage cells
Kaempferia parviflora Wall. ex Baker, is one of the plants in the Zingiberaceae family, locally known in Thai as kra-chai-dam. The rhizome of this plant has been used for treatment of gout, apthous ulcer and abscesses. Since K. parviflora rhizomes have long been used for treatment of inflammation an...
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Published in: | Journal of ethnopharmacology 2008-10, Vol.120 (1), p.81-84 |
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Main Authors: | , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | Kaempferia parviflora Wall. ex Baker, is one of the plants in the Zingiberaceae family, locally known in Thai as kra-chai-dam. The rhizome of this plant has been used for treatment of gout, apthous ulcer and abscesses. Since K. parviflora rhizomes have long been used for treatment of inflammation and possessed marked nitric oxide (NO) inhibitory activity (IC₅₀ =7.8μg/ml), we thus investigated the inhibitory activity of compounds isolated from this plant against lipopolysaccharide (LPS)-induced NO release in RAW264.7 cells. From bioassay-guided fractionation of K. parviflora, seven methoxyflavones were isolated from the hexane fraction and were tested for their anti-inflammatory effects. Among the isolated compounds, compound 5 (5-hydroxy-3,7,3',4'-tetramethoxyflavone) exhibited the highest activity against NO release with an IC₅₀ value of 16.1μM, followed by 4 (IC₅₀ =24.5μM) and 3 (IC₅₀ =30.6μM). Compound 5 was also tested on LPS-induced prostaglandin E₂ (PGE₂) and tumor necrosis factor-alpha (TNF-α) releases from RAW264.7 cells. It was revealed that 5 showed appreciable inhibitory effect on PGE₂ release (IC₅₀ =16.3μM), but inactive on TNF-α (IC₅₀ >100μM). These findings may support the use in Thai traditional medicine of K. parviflora for treatment of inflammatory-related diseases through the inhibition of NO and PGE₂ releases but partly due to that of TNF-α. |
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ISSN: | 0378-8741 1872-7573 |
DOI: | 10.1016/j.jep.2008.07.033 |