• Proceedings of the Korean Vacuum Society Conference
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• 2015.08a
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• pp.158-158
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• 2015

Myoblast are myogenic precursors that proliferate, activate, and differentiate on muscle injury to sustain the regenerative capacity of skeletal muscle; The neuronal isoform of nitric oxide synthase (nNOS, termed also NOS-I) is expressed in normal adult skeletal muscle, suggesting important functions for Nitric oxide (NO) in muscle biology1,2,3. However, the expression and subcellular localization of NO in muscle development and myoblast differentiation are largely unknown. In this study, we examined effects of the nitric oxide generated by a microwave plasma torch, on proliferation/differentiation of rat myoblastic L6 cells. Experimental data pertaining to nitric oxide production are presented in terms of the oxygen input in units of cubic centimetres per minute. The various levels of nitric oxide are observed depending on the flow rate of nitrogen gas, the ratio of oxygen gas, and the microwave power4. In order to evaluate the potential of nitric oxide as an activator of cell differentiation, we applied nitric oxide generated from the microwave plasma torch to L6 skeletal muscles. Differentiation of L6 cells into myotubes was significantly enhanced the differentiation after nitric oxide treatment. Nitric oxide treatment also increase the expression of myogenesis marker proteins and mRNA level, such as myogenin and myosin heavy chain (MHC), as well as cyclic guanosine monophosphate (cGMP), However during the myotube differentiation we found that NO activate oxidative stress signaling erks expression. Therefore, these results establish a role of NO and cGMP in regulating myoblast differentiation and elucidate their mechanism of action, providing a direct link with oxidative stress signalling, which is a key player in myogenesis. Based on these findings, nitric oxide generated by plasma can be used as a possible activator of cell differentiation and tissue regeneration.

• International Journal of Vascular Biomedical Engineering
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• v.1 no.2
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• pp.13-19
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• 2003

Endothelial release of nitric oxide (NO) contributes to the regulation of vascular tone by inducing vascular relaxation. To estimate the blood flow-dependent nitric oxide level and half-life (T1/2) of nitric oxide in vivo state, we investigated the change of aortic NO currents during the change of aortic blood flow rate using NO-selective electrode system and electromagnetic flowmeter in the aorta of anesthetized rats. Resting mean aortic blood flow rate was $49.6{\pm}5.6ml/min$ in the anesthetized rats. NO currents in the aorta were increased by the elevation of blood pressure and/or blood flow rate. When the aortic blood flow was occluded by the clamping, aortic NO currents were decreased. The difference of NO concentration between resting state and occluded state was $1.34{\pm}0.26{\mu}M$ (n=7). This NO concentration was estimated as blood flow-dependent nitric oxide concentration in the rats. Also, while the aortic blood flow was occluded, NO currents were decreased with exponential pattern with $12.84{\pm}2.15$ seconds of time constant and $7.70{\pm}1.07$ seconds of half-life. To summarize, this study suggested that blood flow-dependent NO concentration and half-life of nitric oxide were about $1.3{\mu}M$ and 7.7 seconds, respectively, in the aorta of anesthetized rats. The nitric oxide-selective electrode system is useful for the direct and continuous measurement of NO in vivo state.

• BMB Reports
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• v.41 no.1
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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.

• Proceedings of the Korean Society of Applied Pharmacology
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• 1998.11a
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• pp.145-145
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• 1998

In the present study, we have demonstrated that taurine could stimulate the production of nitric oxide and the activity of ERK2 (extracellular signal regulated protein kinase or pp42 MAP kinase). Nitric oxide(NO), the product of inducible nitric oxide synthase(iNOS), is known to be implicated in the metabolism of bone. ERK cascade plays a key role in the gene expression of iNOS in osteoblastic cell. We investigated whether taurine (l-20mM) could stimulate ERK2 activity, nitric oxide production, and inducible nitric oxide synthase in osteoblast-like UMR-106 cells. Nitric oxide was measured spectophotometrically as nitrite and the activation of ERK2 and iNOS was studied using Western 145 blot analysis. Taurine increased the production of nitric oxide in a dose-dependent manner and the effect was reached to a maximum at 10 mM. The activation of iNOS were consistent with NO levels. The tyrosine phosphorylation of ERK2 was increased by taurine in a time-dependent manner. The these result suggest that taurine might stimulate the production of nitric oxide in osteoblast-like cells by the activation of ERK2 and could regulate the metabolism of bone via nitric oxide.

• Biomolecules & Therapeutics
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• v.18 no.4
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• pp.351-362
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• 2010

Nitric oxide (NO), synthesized from L-arginine by three isoforms of NO synthase (NOS), is a gaseous signaling molecule with an astonishingly wide range of biological and pathophysiological activities, including vasorelaxation, angiogenesis, anti-inflammation, and anti-apoptosis in mammalian cells. Recent studies have shown that NO donors and inhaled NO convert to biologically active NO under biological conditions and act as a signaling molecule in pathophysiological conditions. This review will discuss the roles of NO and its potential therapeutic implication in various human diseases, such as tumor, vascular regeneration, hypertension, wound healing, and ischemia-reperfusion injury.

• Journal of Periodontal and Implant Science
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• v.35 no.4
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• pp.1081-1095
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• 2005

본 연구는 치주질환 주요 병인균주 중의 하나인 Porphyromonas gingivalis의 세균내독소가 마우스 대식 세포주인 RAW264.7 세포에서의 nitric oxide의 생성과 iNOS의 발현에 미치는 영향을 분석하고 그 기전을 규명하기 위해 수행되었다. Butanol추출법과 phenol-water법에 의해 P. gingivalis 381로부터 세균내독소를 추출하였으며, NO의 생성은 배양 상층액 내의 nitrite 농도를 측정하여 결정하였다. 또한, iNOS의 western blot 분석과 reverse transcription (RT)-PCR 산물의 분석을 수행하였다. P. gingivalis의 세균내독소는 부가적인 자극이 없는 상태에서도 iNOS의 발현과 NO 생성을 유발하였으며, NF- ${\kappa}B$, microtubule polymerization, protein tyrosine kinase, 그리고 protein kinase C 등이 P. gingivalis 세균내독소에 의한 NO 생성에 간여하는 것으로 여겨진다. 또한, P. gingivalis 세균내독소에 의한 NO 생성에는 L-arginine이 요구되었다. P. gingivalis 세균내독소에 의한 NO 생성은 염증성 치주질환의 발병과 진행에 있어 중요한 역할을 하는 것으로 여겨진다.

• YAKHAK HOEJI
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• v.42 no.5
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• pp.540-543
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• 1998

The nitric oxide (NO) produced in large amounts by inducible nitric oxide synthase is known to be responsible for the vasodilation and hypotension observed in septic shock. We have found that 8-epi-xanthatin from Xanthium strumarium L. inhibited the production of NO in LPS-activated RAW 264.7 cells ($IC_{50}$ value was 1.5 ${\mu}$M). This activity was resulted from the suppressing of inducible nitric oxide synthase enzyme expression.

• The Korean Journal of Physiology and Pharmacology
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• v.7 no.5
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• pp.283-287
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• 2003

While nitric oxide (NO) produced by inducible nitric oxide synthase (iNOS) is beneficial for host survival, it is also detrimental to the host. Thus, regulation of iNOS gene expression may be an effective therapeutic strategy for the prevention of unwanted reactions at various pathologic conditions. During the screening process for the possible iNOS regulators, we observed that esculetin is a potent inhibitor of cytokine-induced iNOS expression. The treatment of 3T3-L1 adipocytes with the tumor necrosis factor-${\alpha}$ (TNF) induced iNOS expression, leading to enhanced NO production. TNF-induced NO production was inhibited by esculetin in a dose-dependent manner. Esculetin inhibited the TNF-induced NO production at the transcriptional level through suppression of iNOS mRNA and subsequent iNOS protein expression. These results suggest esculetin, a component of natural products, as a naturally occurring, nontoxic means to attenuate iNOS expression and NO-mediated cytotoxicity.

• Korean Journal of Food Science and Technology
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• v.46 no.4
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• pp.511-515
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• 2014

In a screen for plant-derived inhibitors of nitric oxide (NO) production in lipopolysaccharide (LPS)-activated RAW 264.7 macrophage cells, a flavonol isolated from the chloroform extract of Alpinia officinarum was isolated. The structure of the flavonol was found to be 3,5,7-trihydroxy-2-phenylchromen-4-one (galangin, GLG) by using spectroscopy. GLG exhibited an inhibitory effect ($IC_{50}$ value: $26.8{\mu}M$) on NO production in LPS-stimulated RAW 264.7 murine macrophage cells. Moreover, GLG suppressed expressions of inducible nitric oxide synthase (iNOS) protein and mRNA in a dose-dependent manner.

• Journal of Ginseng Research
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• v.22 no.3
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• pp.181-187
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• 1998

Nitric Oxide (NO), derived from L-arginine, is produced by two types (constitutive and inducible) of nitric oxide synthase (NOS). The NO produced in large amounts by the inducible NOS is known to be responsible for the vasodilation and hypotension observed in septic shock. We have found three polyacetylene compounds which inhibited the production of NO in LPS-activated RAW 264.7 cells. Their structures were identified as panauynol, ginsenoyne A and PQ-6 by the spec- troscopic analysis (IC50 values were 32.3 $\mu$M, 2.3 $\mu$M, 1.5 $\mu$M, respectively). These polyacetylenes may be useful candidates for the development of new drug to treat endotoxemia and inflammation accompanied by the overproduction of NO.