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KMID : 1012320060090030152
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Nutritional Sciences
2006 Volume.9 No. 3 p.152 ~ p.158
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Inhibition of Red Ginseng on 5-Hydroxyeicosatetraenoic Acid (5-HETE) Biosynthesis from Arachidonic Acid in Helicobacter Pylori-infected Gastric Cells
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Park Su-Jin
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Abstract
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Helicobacter pylori (H. pylori) infection rapidly stimulated either COX-2 or 5-LOX and released arachidonic acid metabolites that have been considered as pivotal mediators in H. pylori-induced inflammatory responses. To determine whether red ginseng extract (RGE) can suppress the biosynthesis of 5(S)-hydroxyeicosatetraenoic acids (HETE), a precursor metabolite of leukotrienes B4 (LTB4) in H. pylori-provoked inflammatory responses in gastric epithelial cells, the biosynthesis of monohydroxy fatty acids was measured using radioactive arachidonic acid and validated by RP-HPLC using non-radioactive AA as substrate in AGS cells cocultured with H. pylori (ATCC 43504) with or without pretreatment of RGE. Among three known major HETEs, H. pylori infection specifically induced the biosynthesis of 14C-5(S)-HETE rather than the complex of 14C-5S-/14C-12(S)-HETE from 14C-AA, concomitantly obtained by HPLC(p<0.01). RGE, 1 to 100㎍/ml, selectively suppressed H. pylori-stimulated 14C-5(S)-HETE production implying the attenuation of 5-lipoxygenase activity, of which was similar to known LOX inhibitor NDGA(10μM) (p<0.01). However, the amount of 5(S)-HETE was significantly reduced by higher dose of RGE (100㎍/ml) (p<0.05). These results indicated that LOX pathway might be one of principle pathogenic mechanisms of H. pylori and red ginseng could be a nutraceutical against H. pylori infection through inhibiting action of LOX activity.
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KEYWORD
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Helicobactor pylori, Red Ginseng, 5(S)-HETE, LOX, Nutraceutical
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