• The Korean Journal of Physiology and Pharmacology
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• 제2권1호
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• pp.63-68
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• 1998

Nitric oxide (NO)-mediated relaxation in vascular smooth muscle involves not only activation of guanylate cyclase but also hyperpolarization of the membrane. It has been shown that depolarization decreases the [$Ca^{2+}$] sensitivity of myosin light chain kinase in arterial smooth muscle, and nitric oxide (NO)-mediated relaxation was attenuated in this situation. However, why potassium inhibits or attenuates the action of EDRF/NO is not clear. Therefore, we investigated the magnitude of relaxation and cGMP contents using measures known to release NO, such as photorelaxation, photo activated NO-mediated relaxation, and NO-donor (SNP)-mediated relaxation in porcine coronary arterial rings in which contractile conditions were made by different degree of depolarization, i.e., contraction in response to U46619 or U46619 plus KCl. In all cases, the magnitude of relaxation was significantly greater (P＜0.05) in U46619-contracted rings than in U46619+KCl-contracted ones. Although accumulation of cGMP was evident with three measures employed in the present study, no difference was found in cGMP contents between U46619 and U46619+KCl conditions, indicating that the diminished relaxation in KCl containing solution is cGMP-independent mechanism(s). To understand this further, cytosolic $Ca^{2+}$ changes due to NO were compared in rat thoracic aorta by exploiting photoactivated NO using streptozotocin (STZ) that was contracted with either NE or KCl. Fura-3 $[Ca]_{cyt}$ signal caused by NO was small and transient in high $K^+$-, but large and sustained in NE-contracted aorta. The inhibitory potency of STZ expressed in terms of $IC_{50}$ was 5.14 and 3.88 ${\mu}M$ in NE and in high $K^+$, respectively. These results suggest that modification of the cellular mobilization of $Ca^{2+}$ rather than cGMP levels may be an important mechanism for the NO-mediated relaxation when vascular membrane is depolarized, such as atherosclerosis and hypertension.

• The Korean Journal of Physiology and Pharmacology
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• 제4권3호
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• pp.263-270
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• 2000

To evaluate the involvement of nitric oxide production on the endothelium-dependent relaxation in diabetes, we have measured vascular and endothelial function and nitric oxide concentration, and the expression level of endothelial nitric oxide synthase in the streptozotocin-induced diabetic rats. Diabetic rats were induced by the injection of streptozotocin (50 mg/kg i.v.) in the Sprague-Dawley rats. Vasoconstrictor responses to norepinephrine (NE) showed that maximal contraction to norepinephrine $(10^{-5}\;M)$ was significantly enhanced in the aorta of diabetic rats. Endothelium-dependent relaxation induced by acetylcholine was markedly impaired in the aorta of diabetic rats, these responses were little improved by the pretreatment with indomethacin. However, endothelium-independent relaxation induced by nitroprusside was not altered in the diabetic rats. Plasma nitrite and nitrate $(NO_2/_3)$ levels in diabetic rats were significantly lower than in non-diabetic rats. Western blot analysis using a monoclonal antibody against endothelial cell nitric oxide synthase (eNOS) revealed that the protein level was lower in the aorta of diabetic rats than in non-diabetic rats. These data indicate that nitric oxide formation and eNOS expression is reduced in diabetes, and this would, in part, account for the impaired endothelium-dependent relaxation in the aorta of streptozotocin-induced diabetic rats.

• Archives of Pharmacal Research
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• 제23권1호
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• pp.54-58
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• 2000

To elucidate the molecular mechanisms for the suppression of LPS-induced nitric oxide (NO) production by a dehydrocostus lactone (DL) from Saussurea lappa, we examined the preventive effect of this compound on $NF-{\kappa}B$ activation in LPS-treated RAW 264.7 macrophages and U937 human monocytic cells. The results suggest that the suppression of NO production is mediated by the inhibitory action on the i-NOS gene expression through the inactivation of $NF-{\kappa}B$ and this sesquiterpene lactone can act as a pharmacological inhibitor of the $NF-{\kappa}B$ activation.

• 한국독성학회:학술대회논문집
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• 한국독성학회 2001년도 International Symposium on Signal transduction in Toxicology
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• pp.153-153
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• 2001

Nitric oxide (NO) has multifaceted roles in carcinogenesis. Besides acting as an initiator, NO may also playa role in the promotional stage of tumorigenesis or neoplastic transformation. In line with this notion, our previous studies have revealed that the tumor promotor phorbol ester induces expression of inducible nitric oxide synthase (iNOS) and NO production in mouse skin.(omitted)

• 대한약학회:학술대회논문집
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• 대한약학회 2003년도 Proceedings of the Convention of the Pharmaceutical Society of Korea Vol.1
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• pp.268.2-269
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• 2003

Prostaglandins (PGs) and NO (nitric oxide) are important elements to keep homeostasis and host defense system in human beings. When PGs and NO are overproduced by cyclooxygenase-2(COX-2) and inducible nitric oxide synthase (iNOS), respectively, they can cause chronic inflammation, tissue damage, and carcinogenesis. On this line, we are interested in finding agents that can inhibit the production of PGs and NO from natural products for devloping anti-inflammatory and cancer chemopreventive agents. (omitted)

• 동의생리병리학회지
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• 제25권3호
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• pp.540-545
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• 2011

Quercus salicina has been widely used as a traditional medicine for the treatment of various diseases. In macrophages, nitric oxide (NO) is released as an inflammatory mediator and has been proposed to be an important modulator of many pathophysiological conditions in inflammation. In the present study, the inhibitory effect of methanolic extracts of Q. salicina (QSM) on NO production in LPS-stimulated mouse (C57BL/6) peritoneal macrophages was investigated. QSM suppressed NO production without notable cytotoxiciy. QSM also exhibited down-regulation of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) expression via attenuation of NF-${\kappa}B$ translocation to nucleus in rIFN-${\gamma}$ and LPS stimulated mouse peritoneal macrophages. The present study strongly suggest that Q. salicina may be beneficial in diseases which related to macrophage-mediated inflammatory disorders.

• Korean Journal of Acupuncture
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• 제25권3호
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• pp.137-146
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• 2008

Objectives : The leaves of Artemisia argyi L. have been used for the treatment of bleeding-related diseases in traditional korean medicine. But the immunological activities with macrophage have not been sufficiently reported. This study is to investigate the immunological bioactivities of the herbal acupuncture solution obtained from leaves of Artemisia argyi L. (AAAS). Methods & Results : Against Nicotine and Acetaldehyde, AAAS increased significantly the production of hydrogen peroxide (H2O2) within mouse macrophage Raw 264.7 cells above the concentration of 10 ${\mu}g/m{\ell}$. AAAS increased significantly the production of nitric oxide (NO) in Raw 264. 7 cells above the concentration of 100 ${\mu}g/m{\ell}$ against EtOH. And AAAS increased significantly the production of nitric oxide (NO) in Raw 264. 7 cells above the concentration of 200 ${\mu}g/m{\ell}$ against Nicotine, Acetaminophen, and Acetaldehyde. Conclusions : These results suggest that AAAS could be thought to have the immunological activities related with the production of hydrogen peroxide and NO in macrophage.

• 에너지공학
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• 제10권4호
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• pp.379-386
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• 2001

본 연구는 산업용 고부하 버너연소에서의 NO$_{x}$ 저감에 관한 실험적 연구이다. 본 연구에서는 NO$_{x}$의 정량적 농도 분포 측정을 위하여 레이저 유동 형광법을 사용하였다. XeCL 엑시머 레이저를 사용하여 NO A-X (0, 0) 진동밴드를 226 nm로 여기하였다. 또한 P$_{21}$+Q$_1$(14.5)/R$_{12}$+Q$_2$(20.5)/P$_1$(23.5) 전이를 여기라인으로 하였으며 다른 간섭의 영향을 최소화 하였다. 본 실험에서 이중선회 확산화염에서의 NO 농도 분포를 측정하였으며, 이 스월버너에서의 화염의 후류에 있어서 NO 농도는 1차/2차 공기비가 증가할 때 감소함을 알수 있었다.

• 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.

• 약학회지
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• 제42권6호
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• pp.598-606
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• 1998

The liver expresses a considerable amount of nitric oxide (NO) upon induction with cytokines or/and endotoxin. The NO synthesized by inducible NO synthase (NOS) of the liver see ms to play a role in various hepatic physiological processes. Here we investigate the effects of NO on acetaminophen (AA)-induced liver injury. The treatment of S-nitros-N-acetyl penicillamine (SNAP, exogenous NO donor) at the dose of 0.1mM decreased AA-induced hepatotoxicity suggesting the possibility of NO to play a role in protection from the hepatotoxicity induced by AA. On the other hand, the excessive NO produced by NO donor (SNAP: 0.5, 2.5, 6.25mM) has been shown to cause a concentration dependent hepatotoxicity, and such damages was decreased by Superoxide and increased by superoxide dismutase, indicating that the hepatotoxicity induced by excessive NO depends on balancing between NO and superoxide. Taken together, the results indicate that NO has biphasic effects on hepatotoxicity.