• Food Engineering Progress
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• v.15 no.2
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• pp.130-135
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• 2011

Acanthopanax sessiliflorus (A. sessiliflorus) has been known as a traditional medicine having anti-stress, antioxidative and platelet aggregation inhibitory effects. This study was undertaken to investigate the functional properties of water extracts from four parts of A. sessiliflorus. Root, stem, leaf and fruit extracts from A. sessiliflorus were prepared with hot water ($80^{\circ}C$). The contents of functional substances, eleutheroside B and E, polyphenol, antioxidative activity, nitrite scavenging ability and anti-cancer activity of the extracts were determined. The contents of eleutheroside E in stem, root and fruit extracts were 542.50 ${\mu}$g/g, 343.35 ${\mu}$g/g and 30.78 ${\mu}$g/g, respectively. A large part of eleutheroside B was found in fruit (372.01 ${\mu}$g/g) and root (289.33 ${\mu}$g/g) extracts. Root and stem extracts contained 227.21 mg/100g and 131.22 mg/100g of polyphenols, respectively. Antioxidative activities (electron donating ability) of stem and root extracts were 79.87% and 77.27%, respectively. It appears that the antioxidative activities were related to polyphenol contents of the extracts. Most extracts showed 76-81.5% of nitrite scavenging ability at pH 1.2. It reveals that water extract from parts of A. sessiliflorus can inhibit formation of nitrosoamine in food. Effects of the extracts on the growth of normal and cancer cell lines were investigated. Extracts showed no cytotoxicity to normal dendritic cell line (DC2.4). Especially, the root extract promoted the growth of normal cell line. Root and stem extracts had 20-23% of inhibitory effect against stomach cancer cell line (SNU-719) and liver cancer cell line (Hep3B). These result indicated that the extracts from A. sessiliflorus can be used as functional food materials with antioxidative activity and nitrite scavenging ability to eliminate nitrosoamine in food.

• Tuberculosis and Respiratory Diseases
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• v.45 no.6
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• pp.1265-1276
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• 1998

Background : Nitric oxide(NO) is an endogenously produced free radical that plays an important role in regulating vascular tone, inhibition of platelet aggregation and white blood cell adhesion to endothelial cells, and host defense against infection. The highly reactive nature of NO with oxygen radicals suggests that it may either promote or reduce oxidant-induced cell injury in several biological pathways. Oxidant injury and interactions between pulmonary vascular endothelium and leukocytes are important in the pathogenesis of acute lung injury, including acute respiratory distress syndrome(ARDS). In ARDS, therapeutic administration of NO is a clinical condition providing exogenous NO in oxidant-induced endothelial injury. The role of exogenous NO from NO donor or the suppression of endogenous NO production was evaluated in oxidant-induced endothelial injury. Method : The oxidant injury in cultured rat lung microvascular endothelial cells(RLMVC) was induced by hydrogen peroxide generated from glucose oxidase(GO). Cell injury was evaluated by $^{51}$chromium($^{51}Cr$) release technique. NO donor, such as S-nitroso-N-acetylpenicillamine(SNAP) or sodium nitroprusside(SNP), was added to the endothelial cells as a source of exogenous NO. Endogenous production of NO was suppressed with N-monomethyl-L-arginine(L-NMMA) which is an NO synthase inhibitor. L-NMMA was also used in increased endogenous NO production induced by combined stimulation with interferon-$\gamma$(INF-$\gamma$), tumor necrosis factor-$\alpha$(TNF-$\alpha$), and lipopolysaccharide(LPS). NO generation from NO donor or from the endothelial cells was evaluated by measuring nitrite concentration. Result : $^{51}Cr$ release was $8.7{\pm}0.5%$ in GO 5 mU/ml, $14.4{\pm}2.9%$ in GO 10 mU/ml, $32.3{\pm}2.9%$ in GO 15 mU/ml, $55.5{\pm}0.3%$ in GO 20 mU/ml and $67.8{\pm}0.9%$ in GO 30 mU/ml ; it was significantly increased in GO 15 mU/ml or higher concentrations when compared with $9.6{\pm}0.7%$ in control(p < 0.05; n=6). L-NMMA(0.5 mM) did not affect the $^{51}Cr$ release by GO. Nitrite concentration was increased to $3.9{\pm}0.3\;{\mu}M$ in culture media of RLMVC treated with INF-$\gamma$ (500 U/ml), TNF-$\alpha$(150 U/ml) and LPS($1\;{\mu}g/ml$) for 24 hours ; it was significantly suppressed by the addition of L-NMMA. The presence of L-NMMA did not affect $^{51}Cr$ release induced by GO in RLMVC pretreated with INF-$\gamma$, TNF-$\alpha$ and LPS. The increase of $^{51}Cr$ release with GO(20 mU/ml) was prevented completely by adding 100 ${\mu}M$ SNAP. But the add of SNP, potassium ferrocyanate or potassium ferricyanate did not protect the oxidant injury. Nitrite accumulation was $23{\pm}1.0\;{\mu}M$ from 100 ${\mu}M$ SNAP at 4 hours in phenol red free Hanks' balanced salt solution. But nitrite was not detectable from SNP upto 1 mM The presence of SNAP did not affect the time dependent generation of hydrogen peroxide by GO in phenol red free Hanks' balanced salt solution. Conclusion : Hydrogen peroxide generated by GO causes oxidant injury in RLMVC. Exogenous NO from NO donor prevents oxidant injury, and the protective effect may be related to the ability to release NO. These results suggest that the exogenous NO may be protective on oxidant injury to the endothelium.