• Tuberculosis and Respiratory Diseases
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• 제69권5호
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• pp.348-353
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• 2010

Background: In this study, we tried to investigate whether carbenoxolone, prunetin, and silibinin affect tumor necrosis factor (TNF)-${\alpha}$-induced MUC5AC mucin production and gene expression from human airway epithelial cells. Methods: Confluent NCI-H292 cells were pretreated with each agent (carbenoxolone, prunetin, and silibinin) for 30 min and then stimulated with TNF-${\alpha}$ for 24 hours. The MUC5AC mucin gene expression and mucin protein production were measured by reverse transcription-polymerase chain reaction and enzyme linked immunosorbent assay, respectively. Results: Carbenoxolone, prunetin and silibinin inhibited the production of MUC5AC mucin protein induced by TNF-${\alpha}$; the 3 compounds also inhibited the expression of MUC5AC mucin gene induced by TNF-${\alpha}$. Conclusion: This result suggests that carbenoxolone, prunetin and silibinin can inhibit mucin gene expression and production of mucin protein induced by TNF-${\alpha}$, by directly acting on airway epithelial cells.

• Natural Product Sciences
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• 제20권3호
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• pp.196-201
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• 2014

Pyunkang-hwan (Pyunkang-tang) extract (PGT) is a traditional folk medicine for controlling diverse pulmonary diseases including bronchitis, tonsiltis and pneumonitis. We investigated whether PGT significantly affects secretion, production and gene expression of airway mucin using in vivo and in vitro experimental models reflecting the hypersecretion and/or hyperproduction of mucus observed in inflammatory pulmonary diseases. For in vivo experiment, effect of PGT was checked on hypersecretion of pulmonary mucin in sulfur dioxide-induced bronchitis in rats. For in vitro experiment, confluent NCI-H292 cells were pretreated with PGT for 30 min and then stimulated with EGF (epidermal growth factor), PMA (phorbol 12-myristate 13-acetate) or TNF-${\alpha}$ (tumor necrosis factor-${\alpha}$) for 24 h. The MUC5AC mucin gene expression and mucin protein production were measured by RT-PCR and ELISA. The results were as follows: (1) PGT inhibited the expression of MUC5AC mucin gene induced by EGF, PMA or TNF-${\alpha}$ from NCI-H292 cells, respectively; (2) PGT also inhibited the production of MUC5AC mucin protein induced by the same inducers from NCI-H292 cells, respectively; (3) PGT inhibited secretion of mucin in sulfur dioxide-induced bronchitis rat model. This result suggests that PGT can regulate secretion, production and gene expression of airway mucin.

• BMB Reports
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• 제41권1호
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• pp.79-85
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• 2008

The source of nitric oxide (NO) in plants is unclear and it has been reported NO can be produced by nitric oxide synthase (NOS) like enzymes and by nitrate reductase (NR). Here we used wild-type, Atnos1 mutant and nia1, nia2 NR-deficient mutant plants of Arabidopsis thaliana to investigate the potential source of NO production in response to Verticillium dahliae toxins (VD-toxins). The results revealed that NO production is much higher in wild-type and Atnos1 mutant than in nia1, nia2 NR-deficient mutants. The NR inhibitor had a significant effect on VD-toxins-induced NO production; whereas NOS inhibitor had a slight effect. NR activity was significantly implicated in NO production. The results indicated that as NO was induced in response to VD-toxins in Arabidopsis, the major source was the NR pathway. The production of NOS-system appeared to be secondary.

• Environmental Analysis Health and Toxicology
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• 제23권1호
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• pp.33-39
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• 2008

The genotoxicity of mercury compounds have been investigated with a variety of genetic endpoints in prokaryotic and eukaryotic cells. The mercury ions are positively charged and easily form complexes with DNA by binding with negatively charged centers to cause mutagenesis. Further, the mercury ions can react with sulfhydryl (-SH) groups of proteins associated with DNA replication and alter genetic information. Another mechanism by which mercury damages DNA molecule is via its probable involvement of reactive oxygen species (ROS) and induces DNA strand breaks. In order to investigate whether the ROS production was induced by mercury, we performed ROS assay. As the result, the ROS production was significantly increased when it grows dose-dependently and time-dependently. We compared mercury alone-treated group and mercury co-treated with Vitamin C or glutathione group. As the result, the ROS production induced by mercury was decreased by Vitamin C and glutathione. Co-treated with Vitamin C and glutathione group was the most effective to lowering ROS production induced by mercury.

• 약학회지
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• 제45권4호
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• pp.413-418
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• 2001

To investigate action of ATP on ischemia-induced brain injury, we measured phospholipase $A_2$activity and nitric oxide (NO) production in C6 cells. ATP alone did not have any influence on phospholipase $A_2$activity but increased NO production. Glutamate (1 mM) significantly increased phospholipase $A_2$activity whereas did not increased NO production. ATP significantly inhibited phospholipase $A_2$activation induced by 0.1 $\mu$M A23187, 1 mM glutamate and 1 mM $H_2O$$_2$, but did not inhibited 1 $\mu$M PMA-induced phospholipase $A_2$activation. From the above results, it is suggested that the action of ATP in C6 cells has dual actions, such as the inhibition of agonist-induced phospholipase $A_2$activation and the increase of NO production.

• 약학회지
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• 제59권5호
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• pp.215-221
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• 2015

Glucocorticoids are known to have anti-inflammatory effect. To investigate whether corticosterone pretreatment enhances or not lipopolysaccharide (LPS)-induced production of inflammatory mediators, RAW 264.7 cells were pretreated with various concentrations of corticosterone for 24 h and then cultured without corticosterone in the presence or absence of LPS. Our results demonstrated that LPS remarkably increased production of TNF-${\alpha}$, IL-6, IL-$1{\beta}$, vascular endothelial growth factor (VEGF), and NO (nitric oxide). Corticosterone pretreatment significantly attenuated LPS-induced production of TNF-${\alpha}$, IL-$1{\beta}$, and VEGF, while significantly enhanced IL-6 and NO. These findings suggest that corticosterone pretreatment may contribute to LPS-induced inflammatory responses in macrophages via pro- and anti-inflammatory imbalance of inflammatory mediators.

• The Plant Pathology Journal
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• 제29권4호
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• pp.427-434
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• 2013

2R,3R-Butanediol, a volatile compound produced by certain rhizobacteria, is involved in induced drought tolerance in Arabidopsis thaliana through mechanisms involving stomatal closure. In this study, we examined the involvement of nitric oxide and hydrogen peroxide in induced drought tolerance, because these are signaling agents in drought stress responses mediated by abscisic acid (ABA). Fluorescence-based assays showed that systemic nitric oxide and hydrogen peroxide production was induced by 2R,3R-butanediol and correlated with expression of genes encoding nitrate reductase and nitric oxide synthase. Co-treatment of 2R,3R-butanediol with an inhibitor of nitrate reductase or an inhibitor of nitric oxide synthase lowered nitric oxide production and lessened induced drought tolerance. Increases in hydrogen peroxide were negated by co-treatment of 2R,3R-butanediol with inhibitors of NADPH oxidase, or peroxidase. These findings support the volatile 2R,3R-butanediol synthesized by certain rhizobacteria is an active player in induction of drought tolerance through mechanisms involving nitric oxide and hydrogen peroxide production.

• Journal of Plant Biology
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• 제34권4호
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• pp.325-330
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• 1991

The ability of several auxin analogs to induce ethylene production was tested in the corn coleoptile. The synthetic auxins 1-naphthaleneacetic acid (1-NAA) and 2, 4-dichlorophenoxyacetic acid (2, 4-D) had strong stimulatory effects on ethylene induction surpassing that of IAA. Both 2-naphthalaneacetic acid (2-NAA) and 2, 6-dichlorophenoxy acetic acid (2, 6-D), structural analogs of these auxins, respectively, were found to be inactive. Treatment with NPA, a strong inhibitor of polar auxin transport, led to drastic increase in IAA-induced ethylene production while it has bo effect on ethylene production induced by 1-NAA. A positive correlative existed between intracellular auxin level and ethylene production.

• 동의생리병리학회지
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• 제25권2호
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• pp.294-299
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• 2011

The purpose of this study is to investigate effects of Red Ginseng-Ejung-tang (RE) on nitric oxide (NO) and hydrogen peroxide production in RAW 264.7 mouse macrophages induced by lipopolysaccharide (LPS). Cell viability was measured by modified MTT assay. NO production was measured by Griess reagent assay. Hydrogen peroxide production was measured by dihydrorhodamine 123 (DHR) assay. RE did not show cell toxicity against RAW 264.7 for 24 hr incubation at the concentrations of 10, 25, 50, 100, and $200{\mu}g/mL$ in RAW 264.7. RE significantly inhibited NO production for 24 hr incubation at the concentrations of 10, 25, 50, and $100{\mu}g/mL$ in RAW 264.7 (P < 0.05). RE significantly inhibited the LPS-induced production of NO for 24 hr incubation at the concentrations of 10, 25, 50, and $100{\mu}g/mL$ in RAW 264.7 (P < 0.05). RE significantly inhibited the LPS-induced production of hydrogen peroxide for 16, 24, 40, 48, 64, and 72 hr incubation at the concentrations of 50, 100, and $200{\mu}g/mL$ in RAW 264.7 (P < 0.05). These results suggest that RE has anti-inflammatory property related with its inhibition of NO and hydrogen peroxide production in LPS-induced macrophages.

• 대한의생명과학회지
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• 제24권1호
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• pp.50-54
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• 2018

N-nitroso-N-methylurea (NMU) and N-nitroso-N-ethylurea (NEU), direct alkylating chemical mutagens and carcinogens, are shown to be the upregulators of cellular $NF-{\kappa}B$, regulating various genes that mediate tumorigenesis and carcinogenesis. Nitric oxide (NO), a toxic reactive radical gas, has been known to induce programmed cell death or apoptosis in various cells. Therefore, the assessment of NO production was examined to elucidate the possible contribution of NO release to the chemical carcinogenic potency of NMU and NEU in human skin cells. NMU and NEU did not alter the NO production, but they caused a significant downregulation of the NO generation on lipopolysaccharide (LPS)-induced NO production at concentrations ranging from $2{\sim}5{\mu}M$. The degree of downregulation of NO by NMU and NEU decreased up to 15% and 20%, respectively, compared to the control. These results demonstrate that the LPS-inducible keratinocytes NO synthase is involved in modulating carcinogenic potency by NMU and NEU, and the regulation of the cellular $NF-{\kappa}B$ activity by NMU and NEU is negatively correlated with the level of LPS-induced NO production in human skin cells. The findings of this study suggest the hypothesis that NMU and NEU-induced carcinogenesis may be associated with the downregulation of NO production, and the inducible NO may play an important role in NMU and NEU-induced carcinogenicity in human epidermal keratinocytes.