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A NATURAL EXTRACT FROM PIPER PHILIPPINUM (2R,3R)-2-(3',4'-DEHYDROXYBENZYL)-3-(3"-4"-DIMETHOXYBENZYL)BUTYROLACTONE (PP-6) SUPPRESS FMLP-INDUCED SUPDROXIDE PRODUCTION BY INHIBITION FMLP-RECEPTOR BINDING IN HUMAN NEUTORPHIS
Abstract number: P-M-400
Huang1 Y.J., Chen2 I.S., Liao1 C.H.
11Graduate Insitiute of Natural Products, College of Medicine, Chang Gung Uviversity, Tao-Yuan 22College of Pharmacy, Graduate Insitiute of Natural Products, Kaohsiung, Taiwan
How-to-cite Huang YJ, Chen IS, Liao CH. A NATURAL EXTRACT FROM PIPER PHILIPPINUM (2R,3R)-2-(3',4'-DEHYDROXYBENZYL)-3-(3"-4"-DIMETHOXYBENZYL)BUTYROLACTONE (PP-6) SUPPRESS FMLP-INDUCED SUPDROXIDE PRODUCTION BY INHIBITION FMLP-RECEPTOR BINDING IN HUMAN NEUTORPHIS. J Thromb Haemost 2007; 5 Supplement 2: P-M-400
Abstract
Introduction: The purpose of the present work was to investigate the mechanism underlying the inhibitory action of (2R,3R)-2-(3',4'-Dihydroxybenzyl)-3-(3",4"-dimethoxybenzyl)butyrolactone (PP-6), an extracted from Piper Philippinum, on superoxide anion production by the fMLP in human neutrophil.
Methods: Flow cytometer was used to analysis the free radical production, surface marker expression and fMLP receptor binding. Western blotting was used to analysis the intracellular signanling, such as ERK phosphorylation.
Results: fMLP (1 muM), PMA (100 ng/ml) or leukotriene B4 (1 muM) induced superoxide anion release in human neutrophils. PP-6 specific inhibited fMLP induced superoxide anion production in human neutrophil with a concentration dependent manner. The IC50 value for PP-6 on fMLP induced superoxide anion was 0.30.1muM. However, PP-6 did not affect the free radical production caused by PMA or leukotriene B4. PP-6 did not increase cyclic nucleotide whcih was report inhibted fMLP induced free radical. PP-6 also specific inhibited fMLP induced intracellular signaling, such as intracellular calcium mobilization and ERK (p42/p44) phosphorylation. Moreover, PP-6 specific inhibited fMLP induced Mac-1 expression. PP-6 inhibited FITC-fMLP binding to neutrophil with a concentration dependent manner. The IC50 value for PP-6 on FITC-fMLP binding was 1.50.2 muM. This data showed that PP-6 inhibited the binding of fMLP to fMLP receptor on human neutrophils. PP-6 did not parallel shift the concentration response of fMLP induced superoxide anion. This data indicated that PP-6 inhibited fMLP binding to fMLP receptor with a non-competitive manner. Furthermore, the inhibitory effect of PP-6 on fMLP induced superoxide anion was reversed when PP-6 was washed out.
Conclusions: These results provide evidence that a natural product, PP-6, inhibited fMLP binding to fMLP receptor with a not-competitive and reversed manner.
To cite this abstract use the following format:
Journal of Thrombosis and Haemostasis 2007; Volume 5, Supplement 2: abstract number
Session Details
| Date: |
01/08/2007
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| Time: |
00:00-00:00
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| Session name: |
XXIst ISTH Congress |
| Subject: |
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| Location: |
Oxford, UK |
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