• Nutritional Sciences
• /
• 제9권3호
• /
• pp.152-158
• /
• 2006

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 $^{14}C-5(S)-HETE$ rather than the complex of $^{14}C-15S-/^{14}C-12(S)-HETE$ from $^{14}C-AA$, concomitantly obtained by HPLC(p<0.01). RGE, 1 to $100{\mu}g/ml$, selectively suppressed H. pylori-stimulated $^{14}C-5(S)-HETE$ production implying the attenuation of 5-lipoxygenase activity, of which was similar to known LOX inhibitor NDGA $(10{\mu}M)$ (p<0.01). However, the amount of 5(S)-HETE was significantly reduced by higher dose of RGE $(100{\mu}g/ml)$ (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.

• 한국식품과학회지
• /
• 제29권2호
• /
• pp.355-361
• /
• 1997

털없는 쥐표피를 적출하여 ultraviolet B로서 조사한 후 녹차의 열수 추출물이 표피의 효소의 활성에 대한 항산화 효과를 조사하였다. 녹차의 열수추출물을 5, 25, 50 및 $100\;{\mu}g$으로 쥐표피에 첨가한 후 ultraviolet B을 $1.0\;joule/cm^{2}$로 조사한 후 효소활성을 조사한 결과 catalase와 glutathione reductase는 녹차의 열수 추출물의 첨가용량이 증가할수록 영향을 미치는 것으로 나타났으나 glutathione peroxidase와 superoxide dismutase는 영향을 받지 않았다. 한편 lipoxygenase의 활성을 알아보기 위하여 arachidonic acid에 $50\;{\mu}g$ 녹차의 열수 추출물을 첨가하여 대사를 검토한 결과 대사산물 12 또는 15-hydroxyeicosa- tetraenoic acid보다 5-HETE 및 8-HETE가 억제되었다. 녹차의 열수 추출물을 5, 25, 50 및 $100\;{\mu}g$ 첨가하였을 때 5-HETE는 각각 32, 52, 62 및 80% 억 제되었고 8-HETE는 각각 36, 47, 70 및 84%로 억제됨을 알 수 있었다.

• Archives of Pharmacal Research
• /
• 제25권6호
• /
• pp.747-758
• /
• 2002

The skin displays a highly active metabolism of polyunsaturated fatty acids (PUFA). Dietary deficiency of linoleic acid (LA), an 18-carbon (n-6) PUFA, results in characteristic scaly skin disorder and excessive epidermal water loss. Although arachidonic acid (AA), a 20-carbon (n6) PUFA, is metabolized via cyclooxygenase pathway into predominantly prostaglandin $E_2(PGE_2)$ and $PGF_{2{\alpha}}$, the metabolism of AA via the 15-lipoxygenase (15-LOX) pathway, which is very active in skin epidermis and catalyzes the transformation of M into predominantly 15S-hydroxyeicosatetraenoic acid (15S-HETE). Additionally, the 15-LOX also metabolizes the 18-carbon LA into 13S-hydroxyoctadecadienoic acid (13S-HODE), respectively. Interestingly, 15-LOX catalyzes the transformation of $dihomo-{\gamma}-linolenic$ acid (DGLA), derived from dietary gamma-linolenic acid, to 15S-hydroxyeicosatrienoic acid (15S-HETrE). These monohydroxy fatty acids are incorporated into the membrane inositol phospholipids which undergo hydrolytic cleavage to yield substituted-diacylglycerols such as 13S-HODE-DAG from 13S-HODE and 15S-HETrE-DAG from 15S-HETrE. These substituted-monohydroxy fatty acids seemingly exert anti-inflammatory/antiproliferative effects via the modulation of selective protein kinase C as well as on the upstream/down-stream nuclear MAP-kinase/AP-1/apoptotic signaling events.