• Environmental Mutagens and Carcinogens
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• v.26 no.1
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• pp.7-11
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• 2006

Reactive oxygen species (ROS) are known to cause oxidative modification of DNA, proteins, lipids and small cellular molecules and are associated with tissue damage and are the contributing factors for diabetes, inflammation, aging, cancer, arteriosclerosis, and hypertension. We screened the anti-oxidative effect on V79-4 hamster lung fibroblast cells induced by hydrogen peroxide with eleven extracts of combined medicinal plants. Dancheonhwankakambang and Samikangyabtang were found to show the scavenging activities of DPPH radical and intracellular reactive oxygen species, which is measured by dichlorodihydrofluorescin diacetate method (DCHF-DA).

• Preventive Nutrition and Food Science
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• v.14 no.1
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• pp.49-53
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• 2009

Antioxidative activities of major pentacyclic terpenoids from the semi-fermented tea of Camellia sinensis L. were investigated. The free radical scavenging activities of triterpenoids $1{\sim}3$ were examined with of DPPH and superoxide anion radical scavenging activity. The $IC_{50}$ of compounds 1 and 2 for DPPH radical scavenging activities were 23.1 and $37.2{\mu}g/mL$ respectively, and for superoxide anion radical scavenging activities were 37.2 and $35.2{\mu}g/mL$, respectively. According to this result, compounds 1 or 2 in semi-fermented tea could be the candidates for bioactive material having antioxidant activity.

• Toxicological Research
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• v.25 no.4
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• pp.159-173
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• 2009

Nuclear factor erythroid derived 2-related factor-2 (Nrf2) is a master transcription regulator of antioxidant and cytoprotective proteins that mediate cellular defense against oxidative and inflammatory stresses. Disruption of cellular stress response by Nrf2 deficiency causes enhanced susceptibility to infection and related inflammatory diseases as a consequence of exacerbated immune-mediated hypersensitivity and autoimmunity. The cellular defense capacity potentiated by Nrf2 activation appears to balance the population of $CD4^+$ and $CD8^+$ of lymph node cells for proper innate immune responses. Nrf2 can negatively regulate the activation of pro-inflammatory signaling molecules such as p38 MAPK, NF-${\kappa}B$, and AP-1. Nrf2 subsequently functions to inhibit the production of pro-inflammatory mediators including cytokines, chemokines, cell adhesion molecules, matrix metalloproteinases, COX-2 and iNOS. Although not clearly elucidated, the antioxidative function of genes targeted by Nrf2 may cooperatively regulate the innate immune response and also repress the expression of pro-inflammatory mediators.

• Proceedings of the PSK Conference
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• 2003.04a
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• pp.183.2-184
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• 2003

Zinc is known to have an inhibitory effect on apoptosis and an antioxidative effect scavenging reactive oxygen species (ROS) under oxidative stress. We studied the influence of zinc on cadmium-induced apoptosis especially associated with ROS in MCF-7 human breast carcinoma cell line. For the determination of appropriate experimental concentration and time, we excecuted MTT [3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide] assay and DNA fragmentation assay. (omitted)

• Proceedings of the Korean Society of Toxicology Conference
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• 2003.05a
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• pp.91-92
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• 2003

Oxidative stress induced by reactive oxygen intermediates (ROIs) has been implicated in a variety of human diseases including cancer, diabetes, rheumatoid arthritis and neurodegenerative disorders. Hydrogen peroxide ($H_2O$$_2$), a representative ROI which is produced during the cellular redox process, can cause cell death via apoptosis and/or necrosis depending on its concentrations. (omitted)

• Journal of Nutrition and Health
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• v.29 no.2
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• pp.223-231
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• 1996

To investigate antioxidant status and platelet antioxidative enzyme activity in patients with ischemic heart disease, 36 male patients admitted to Kyungpook National University Hospital from June to December 1994 were compared to 36 healthy male control subjects. The percentages of heavy smoking and nonexercise were significantly higher in the patient group compared to the control, but the drinking status was not significantly different between groups. Food habit and food frequency scores were significantly lower in patients than in control subjects. Plasma retinol levels tended to be lower in the patient group, and plasma $\alpha$-tocopherol and $\beta$-carotene levels were not different between groups. There was no difference in the level of plasma thiobarbituric acid reactive substances(TBARS) and in the activities of platelet glutathione peroxidase and catalase. Our results indicate that oxidative stress, which is reflected by the plasma levels of antioxidants and TBARS, did not increase in the patients with ischemic heart disease, and the long-term effects due to smoking, poor food habit and other life styles could possibly contribute to the onset of the disease.

• Journal of Community Nutrition
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• v.8 no.4
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• pp.207-213
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• 2006

The present study was conducted to investigate the effect of oolong tea extract on blood glucose level and antioxidant system in diabetic rats. The Sprague-Dawley rats were fed on AIN-76 based experimental diets containing 1 % oolong tea extract for 6 weeks. They were induced to be diabetic by receiving streptozotocin (45mg/kg BW) intramuscularly. Blood glucose, blood and hepatic concentration of vitamins A and E, and antioxidant enzyme activities were measured. Oolong tea extract feeding decreased the plasma glucose in diabetic rats. Dietary supplementation of oolong tea extract did not affect antioxidative enzyme activities such as superoxide dismutase, glutathione peroxidase and catalase in diabetic rats. The plasma level of retinol was increased in diabetic rats by feeding oolong tea extract. Plasma and hepatic levels of ${\alpha}$-tocopherol were higher in diabetic rats fed oolong tea extract. In conclusion, these results suggest that oolong tea extract consumption might reduce the plasma glucose in diabetic rats and protect the oxidative damage from diabetic stress to some extent.

• 한국약용작물학회:학술대회논문집
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• 2010.10a
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• pp.339-340
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• 2010

• Proceedings of the Korean Society of Life Science Conference
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• 2007.10a
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• pp.110.1-110.1
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• 2007

See Full Text

• 한국약용작물학회:학술대회논문집
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• 2009.05a
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• pp.215-216
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• 2009