• The korean journal of orthodontics
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• v.36 no.6
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• pp.465-473
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• 2006

Objective: This study evaluated the effects of nitric oxide (NO) on the proliferation and differentiation of human periodontal ligament cells involved in orthodontic tooth movement. Methods: A range of concentrations of sodium nitroprusside (SNP), a NO donor, were administered to samples of human periodontal ligament cells, followed by measurement of cell viability, alkaline phosphatase (ALP) activity, and expression of osteonectin and bone sialoprotein. Results: Cell viability, ALP activity and the expression of osteonectin and bone sialoprotein were increased in human periodontal ligament cells treated with SNP concentrations of < 0.2 mM compared with controls, but were decreased with SNP concentrations of > 1.0 mM. Conclusion: NO has a biphasic effect on proliferation and differentiation in human periodontal ligament cells, with a stimulatory effect at low concentrations and an inhibitory effect at high concentrations.

• Korean Journal of Agricultural Science
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• v.39 no.4
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• pp.467-471
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• 2012

In this study, we investigated the antioxidative and antiaging activity of Perilla frutescens using LLC-$PK_1$ porcine renal epithelial cell and WI-38 human diploid fibroblast cell. The extract from Perilla frutescens showed strong protective effect against nitric oxide (NO) and superoxide ($O_2{^-}$)-induced oxidative stress generated by sodium nitroprusside (SNP) and pyrogallol, respectively. The result showed that P. frutescens increased the cell viability and showed scavenging activity of NO and $O_2{^-}$. In addition, the extract of P. frutescens exerted the protective effect against peroxynitrite ($ONOO^-$) induced by 3-morpholinosydnonimine. It suggests that P. frutescens would have the protective role against $ONOO^-$ itself and its precursors, NO and $O_2{^-}$. Furthermore, the aging model of hydrogen peroxide ($H_2O_2$)-treated WI-38 human diploid fibroblast was employed to investigate the anti-aging effect of P. frutescens. $H_2O_2$-treated WI-38 cells showed the loss of cell viability, however before-treatment with P. frutescens to WI-38 cells under premature senescence could delay the cellular aging process. The present study suggests the antioxidative and antiaging potential against free radical-induced oxidative damage of P. frutescens.

• The Korean Journal of Zoology
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• v.36 no.3
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• pp.433-438
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• 1993

In the previous paper (Choi et al., 1992), we found that a large but transient elevation in intracellular cGMP levels occur concomitant with the myoblast fusion. To establish the physiological significance of the elevation of cGMP levels, the change in guanylate cyclase activity dudng myoblast fusion and the correlation hetween various chemicals that may affect guanylate cyclase adivity and myoblast fusion were examined. Sodium nitroprusside, a nitric oxide-forming compound, induced a precocious fusion and increased guanylate cyclase activity compared to the control. Furthermore, L-NG-monomethyl arginine, specific inhibitor of L-arginine: nitric oxide synthase, inhibited the cell fusion in a dose-dependent manner, without affecting biochemical differentiation. On the basis of our present findings, we propose that the onset of myoblast fusion is somehow correlated with the rise in cellular cGMP levels that is regulated by the activation or inhibItIon of soluble guanylate cyclase, via as yet undefined mechanism but possibly through L-arginine: nitric oxide pathway.

• Journal of Acupuncture Research
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• v.22 no.2
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• pp.123-132
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• 2005

Melittin,cationic 26-amino acid, is the principal component of the bee venom (BV) which has been used for treatment of inflammatory disease such as arthritis rheumatism NF-kB is activated by subsequent release of inhibitory IkB via activation of a multisubunit IkB kinase (IKK). We previously found that melittin bind to the sulfhydryl group of p50, a subunit of NF-kB. Since sulfhydryl group is present in kinase domain of IKKa and IKKb, melittin could modify IKK activity by protein-protein interaction. We therefore examined effect of melittin on IKK activities in sodium nitroprusside (SNP)-stimulated synoviocyte obtained from RA patients. Melittin suppressed the SNP-induced release of IkB resulted in inhibition of DNA binding activity of NF-kB and NF-kB-dependent luciferase activity. Consistent with the inhibitory effect on NF-kB activation, IKKa and IKKb activities were also suppressed by melittin. Surface plasmon resonance analysis realized that melitin binds to IKKa $(Kd\;=\;1.34{\times}10-9M)$ and IKKb$(Kd\;=\;1.0{\times}10-9M)$. Inhibition of IKKa and IKKb resulted in reduction of the SNP-induced production of inflammatory mediators NO and PGE2 generation. The inhibitory effect of melittin on the IKKs activities, binding affinity of melittin to IKKs, and NO and PGE2 generation were blocked by addition of reducing agents dithiothreitol and glutathione. In addition, melittin did not show inhibitory effect in the transfected Synoviocytes with plasmid carrying dominant negative mutant IKKa (C178A) and IKKb (C179A). These results demonstrate that melittin directly binds to sulfhydryl group of IKKs resulting in IkBrelease, thereby inhibits activation of NF-kB and expression of genes involving in the inflammatory responses.

• The Korean Journal of Physiology
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• v.29 no.1
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• pp.39-50
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• 1995

This study was designed to clarify the action of cyclic nucleotides, cyclic AMP and cyclic GMP, on phorbol 12,13-dibutyrate (PDBu)-induced contraction in rings isolated from rabbit carotid artery. Arterial rings, 2 mm in width, were myographied isometrically in an isolated organ bath. PDBu produced slowly developing, sustained contraction in rabbit carotid artery, in a dose dependent manner, which was independent of extracellular $Ca^{2+}$ PDBu-induced contraction was relaxed by staurosporine, which suggests that PDBu-induced contraction is mediated by protein kinase C (PKC). $^{45}Ca^{2+}$ uptake by rabbit carotid artery was increased by PDBu during depolarization, but not in control. Isoproterenol and sodium nitroprusside (SNP) relaxed phenylephrine-induced contraction. However, SNP but not isoproterenol relaxed the contraction induced by PDBu. Acetylcholine relaxed PDBu-induced contraction in the presence of the endothelium. 8-bromo-cyclic AMP, a permeable analogue of cyclic AMP, suppressed phenylephrine-induced contraction but not PDBu-induced contraction. 8-bromo cyclic GMP relaxed both of them with dose dependency. A large dose of forskolin relaxed PDBu-induced contraction. PDBu increased cyclic AMP without considerable change in the level of cyclic GMP. Based on these findings, PDBu-induced contraction of rabbit carotid artery was relaxed by cyclic GMP more effectively than cyclic AMP, and the action of cyclic AMP could be mediated by cyclic GMP dependent protein kinase. Therefore it is suggested that the antagonistic action between protein kinase C and cyclic GMP-dependent protein kinase plays a major role in the regulation of vascular tone.

• The Korean Journal of Physiology
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• v.29 no.1
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• pp.51-59
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• 1995

This study was designed to test whether or not 1) ischemia-reperfusion attenuates endothelium-dependent relaxation of coronary arteries and 2) preconditioning protects the arterial endothelium from ischemia-reperfusion injury. In anesthetized open chest rabbits, branches of the left circumflex artery were exposed to different combinations of the experimental conditions; ischemia (15 minutes), ischemia (15 minutes)-reperfusion (10 minutes), preconditioning ischemia, and pre-conditioning fellowed by ischemia-reperfusion. Preconditioning consisted of 3 occlusions of 2-min duration, each followed by n 5-min reperfusion. Rings of the artery exposed to the experimental condition and of normal left anterior descending coronary artery were prepared and suspended for isometric force measurement in organ chambers containing Krebs Ringer bicarbonate solution. The rings were contracted with 29.6 mM KCI. Ischemia alone did not attenuate endothelium-dependent relaxation by acetylcholine. However, ischemia-reperfusion significantly impaired endothelium-dependent relaxation. Endothelium-independent relaxation by sodium nitroprusside was not impaired by ischemia-reperfusion and the constrictive response to acetylcholine was not altered in reperfused rings without endothelium, compared with control rings. Arterial rings exposed to preconditioning followed by ischemia-reperfusion exhibited impaired endothelium-dependent relaxation by acetyl-choline. However, although preconditioning not fellowed by ischemia-reperfusion, attenuated endothelium-dependent relaxation at low concentrations of acetylcholine, the magnitude of the impairment by preconditioning followed by ischemia-reperfusion was significantly less than that of the impairment by ischemia-reperfusion alone. These data demonstrate that ischemia-reperfusion significantly attenuates endothelium-dependent relaxation by producing endothelial dysfunction and preconditioning Protects the endothelium of coronary arteries from ischemia-reperfusion injury.

• Journal of Microbiology
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• v.43 no.1
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• pp.44-48
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• 2005

In our previous study, the first structural gene (GGTI) encoding ${\gamma}-glutamyl$ transpeptidase was cloned and characterized from the fission yeast Schizosaccharomyces pombe, and its transcription, using the GGTI-lacZ fusion gene, containing the 1,085 bp upstream region from the translational initiation point, was found to be enhanced by sodium nitroprusside and L-buthionine-(S,R)-sulfoximine (BSO). In the present work, regulation of the GGTI gene was further elucidated. Non-fermentable carbon sources, such as acetate and ethanol, markedly enhanced the synthesis of ${beta}-galactosidase$ from the GGTI-lacZ fusion gene. However, its induction by non-fermentable carbon sources appeared to be independent of the presence of the Pap1 protein. Nitrogen starvation also gave rise to induction of GGTI gene expression in a Pap1-independent manner. The three additional fusion plasmids, carrying 754, 421 and 156 bp regions, were constructed. The sequence responsible for the induction by non-fermentable carbon sources and nitrogen starvation was identified to exist within a -421 bp region of the GGTI gene. Taken together, the S. pombe GGTI gene is regulated by non-fermentable carbon sources and nitrogen starvation.

• The Korean Journal of Physiology and Pharmacology
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• v.10 no.6
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• pp.329-335
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• 2006

This study was aimed to investigate the nitric oxide (NO)-induced cytotoxic mechanism in PC12 cells. Sodium nitroprusside (SNP), an NO donor, decreased the viability of PC12 cells in dose-and time-dependent manners. SNP enhanced the production of reactive oxygen species (ROS), and gave rise to apoptotic morphological changes including cell shrinkage, chromatin condensation, and DNA fragmentation. Expression of Bax was not affected, whereas Bcl-2 was downregulated in SNP-treated PC12 cells. SNP augmented the release of cytochrome c from mitochondria into cytosol and enhanced caspase -8, -9, and -3 activities. SNP upregulated both Fas and Fas-L, which are known to be components of death receptor assembly. These results suggest that NO induces apoptosis of PC12 cells through both mitochondria-and death receptor-mediated pathways mediated by ROS and Bcl-2 family.

• Toxicological Research
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• v.12 no.2
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• pp.195-201
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• 1996

Endotoxic shock causes death in humans and animals via extreme hypoperfusion of peripheral organs. A massive production of nitric oxide (NO) both from the endothelical cells and smooth muscle cells has been proposed as a possible mechanism in this process. Since NO attenuated the contractility to vasoconstricting agents such as norepinephrine (NE) by directly acting on the smooth muscle cells, this mechanism was considered mainly as a postsynaptic mechanism. In this research it was investigated whether NO, thus released, also participates in the presynaptic events for the regulation of vascular tone in endotoxic shock. The role of NO was studied by adding NO donors or NO synthase inhibitor $N^\omega $methyl-L-arginine (NMA) in stimulated sympathetic nerves of the mesenteric vascular bed and the Langendorff heart of rats. Sodium nitroprusside (SNP), an NO donor, reduced the pressor responses of isolated mesenteric artery either to electrical stimulation or exogenously administered phenylephrine (PE). In this mesentery, although neither agent influenced NE release, in the presence of the adrenergic $\alpha_2$-receptor antagonist yohimbine, elecrical stimulation-evoked NE release was augumented by SNP. In the heart SNP facilitated the NE release induced by electrical stimulation, while NMA had no effect. From these results it is proposed that there exists a local reflex phenomenon in the junction between the sympathetic nerve terminals and the smooth muscle of resistance blood vessels; by which sympathetic responses are reduced by NO at the postjunctional level while NO facilitates NE release contributing to augumentation of sympathetic tone. All these facts suggest that NO produced during endotoxic shock has dual effects: whereas NO blunts the vasoconstrictive activity of NE at the postsynaptic level, NO presynaptically facilitates the release of NE from sympathetic nerve terminals.

• The Korean Journal of Mycology
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• v.47 no.3
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• pp.219-232
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• 2019

Chemicals related to hydrogen peroxide ($H_2O_2$) and nitric oxide (NO) generations were exogenously applied to Fusarium oxysporum f. sp. fragariae (Fof) causing Fusarium wilt disease in strawberry plants, and regulations of in vitro conidial germination and mycelial growth of the fungus by the chemical treatments were evaluated. $H_2O_2$ drastically reduced the conidial germination of Fof in a dose-dependent manner, and treatment with 3-amino-1,2,4-triazole (3-AT) catalase inhibitor also led to dose-dependent inhibition of conidial germination but relatively moderately. Gradual decreases in mycelial growth of Fof were found by high concentrations of $H_2O_2$, whilst exogenous 3-AT slightly increased the mycelial growth. Increasing sodium nitroprusside (SNP) NO donor, $N^G$-nitro-l-arginine methyl ester (L-NAME) NO synthase (NOS)-inhibitor and tungstate nitrate reductase (NR) inhibitor led to dose-dependent reductions in conidial germination of Fof in quite different levels. SNP conversely increased the mycelial growth but increasing L-NAME moderately decreased the mycelial growth. Tungstate strongly enhanced mycelial growth. Differentially regulated in vitro mycelial growths of Fof were demonstrated by SNP, L-NAME and tungstate with or without $H_2O_2$ supplement. Superoxide anion production was also regulated during the mycelial growth of Fof by nitric oxide. These results show that $H_2O_2$ and NO-associated enzymes can be suggested as fungal growth regulators of Fof as well as eco-friendly disease-managing agents in strawberry production fields.