• Title/Summary/Keyword: Nitric

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Immunohistochemical Changes of Apoptotic Control Genes by Chronic Inhibition of Nitric Oxide in Rats

  • Bae, Hyung-Joon
    • Biomedical Science Letters
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    • v.18 no.4
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    • pp.420-427
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    • 2012
  • Sprague-Dawley (SD) rats were orally administered with NG-nitro-L-arginine methyl ester (L-NAME), which inhibits or blocks the production of nitric oxide from L-arginine in vascular endothelial cells and vessel tissue. We examined the effects of nitric oxide on some physiological changes such as blood pressure and heart rate, and confirms the apoptosis induced by the suppressed nitric oxide activity in the kidney. This study was performed to investigate correlation between the activities of nitric oxide and apoptosis by immunohistochemical changes of apoptotic control proteins with regulated chronic inhibition of nitric oxide. In the kidney from L-NAME-treated group, immunohistochemical reaction to the antigens of apoptosis inhibiting proteins such as bcl-2 and bcl-xL, exhibited a time-dependent reduction. The expression of apoptosis-inhibiting proteins such as bax and p53 increased expression in proportion to the duration of treatment. The most sensitive apoptosis regulating proteins to L-NAME were p53 in stimulation and bcl-2 in inhibition, respectively.

Inhibition of Nitric Oxide Synthesis by 8-epi-xanthatin in Activated RAW 264.7 Cells (활성화한 RAW 264.7 세포주에서 8-epi-xanthatin의 Nitric Oxide 생성저해)

  • Lee, Hwa-Jin;Jeong, Yeon-Su;Ryu, Shi-Yong;Ryu, Jae-Ha
    • 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.

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Inhibition of TCDD Induced Cyplal Expression by SNP In Hepa I Cells

  • Kim, Ji-E.;Sheen, Yhun-Y.
    • Biomolecules & Therapeutics
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    • v.7 no.4
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    • pp.315-321
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    • 1999
  • Since it has been known that hypoxia increases inducible nitric oxide synthase (iNOS) gene expression through hypoxia responsive element, it was possible to establish the hypothesis that nitric oxide could be a mediator of hypoxia to inhibit Cyplal promoter activity. In order to test this hypothesis, we have undertaken the study to examine the effects of hypoxia and nitric oxide on Cyplal promoter activity in Hepa I cells. Mouse Cyplal 5'flanking DNA, 1.6 Kb was cloned into pGL3 expression vector in order to construct pmCyplal-Luc. Hepa I cells were transfected with pmCyplal-Luc and were treated with $10^{-9}$ M TCDD and nitric oxide producing agents, such as lipopolysaccharide(LPS), sodium nitroprusside (SNP). Luciferase activity of reporter gene was measured from pmCyplal-Luc transfected Hepa I cell lysate which contains 2 g total protein using luciferin as a substrate. Nitric oxide producing agents, such as lipopolysaccharide (LPS), sodium nitroprusside(SNP) showed inhibition of luciferase activity that was induced by $10^{-9}$M TCDD treatment with dose dependent manner. Concomitant treatment of 1mM $N^G$-nitro-ι-arginine with $10^{-6}$~$10^{-4}$M sodium nitro-prusside recovered luciferase activity from the TCDD induced luciferase activity that was inhibited by nitric oxide producing agents. These demonstrated that nitric oxide could be a mediator of inhibitors on dioxin induced Cyplal expression in Hepa I cells.

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Effect of Cnidii Rhizoma on Proliferation of Breast Cancer Cell, Nitric Oxide Production and Ornithine Decarboxylase Activity (천궁이 유방암세포 증식, Nitric Oxide 생성 및 Ornithine Decarboxylase 활성에 미치는 영향)

  • Nam, Kyung-Soo;Son, Ok-Lye;Lee, Kyung-Hwa;Cho, Hyun-Jung;Shon, Yun-Hee
    • Korean Journal of Pharmacognosy
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    • v.35 no.4 s.139
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    • pp.283-287
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    • 2004
  • The effect of water extract from Cnidii Rhizoma (CRW) on proliferation of human breast cancer cells, nitric oxide production, nitric oxide synthase expression, and ornithine decarboxylase activity was tested. CRW inhibited the growth of both estrogen-dependent MCF-7 and estrogen-independent MDA-MB-23I human breast cancer cells. Lipopolysaccharide-induced nitric oxide (NO) production was significantly reduced by CRW at the concentration of 0.5, 1.0 and 5.0 mg/ml. Expression of inducible nitric oxide synthase (iNOS) was also suppressed with the treatment of CRW in Raw 264.7 cells. CRW inhibited induction of ornithine decarboxylase by 12-0-tetradecanoylphorbol-13-acetate, a key enzyme of polyamine biosynthesis, which is enhanced in tumour promotion. Therefore, CRW is worth further investigation with respect to breast cancer chemoprevention or therapy.

Nitric Oxide and Hydrogen Peroxide Production are Involved in Systemic Drought Tolerance Induced by 2R,3R-Butanediol in Arabidopsis thaliana

  • Cho, Song-Mi;Kim, Yong Hwan;Anderson, Anne J.;Kim, Young Cheol
    • The Plant Pathology Journal
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    • v.29 no.4
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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.

Protective Mechanism of Nitric Oxide and Mucus against Ischemia/Reperfusion-Induced Gastric Mucosal Injury

  • Kim, Hye-Young;Nam, Kwang-Soo;Kim, Kyung-Hwan
    • The Korean Journal of Physiology and Pharmacology
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    • v.2 no.4
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    • pp.511-519
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    • 1998
  • This study investigated the role of nitric oxide on the oxidative damage in gastric mucosa of rats which received ischemia/reperfusion and its relation to mucus. Nitric oxide synthesis modulators such as L-arginine and $N^G-nitro-L-arginine$ methyl ester, and sodium nitroprusside, a nitric oxide donor, were injected intraperitoneally to the rats 30 min prior to ischemia/reperfusion which was induced by clamping the celiac artery and the superior mesenteric artery for 30 min and reperfusion for 1 h. Lipid peroxide production, the contents of glutathione and mucus, and glutathione peroxidase activities of gastric mucosa were determined. Histological observation of gastric mucosa was performed by using hematoxylin-eosin staining and scanning electron microscopy. The result showed that ischemia/reperfusion increased lipid peroxide production and decreased the contents of glutathione and mucus as well as glutathione peroxidase activities of gastric mucosa. Ischemia/reperfusion induced gastric erosion and gross epithelial disruption of gastric mucosa. Pretreatment of L-arginine, a substrate for nitric oxide synthase, and sodium nitroprusside prevented ischemia/reperfusion-induced alterations of gastric mucosa. However, $N^G-nitro-$ L- arginine methyl ester, a nitric oxide synthase inhibitor, deteriorated oxidative damage induced by ischemia/reperfusion. In conclusion, nitric oxide has an antioxidant defensive role on gastric mucosa by maintaining mucus, glutathione, and glutathione peroxidase of gastric mucosa.

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Nitric acid leaching of electronic scraps and the removal of free nitric acid from the leaching solution for the recovery of copper and tin. (전자(電子)스크랩에서 구리 및 주석의 회수(回收)를 위한 질산(窒酸) 침출(浸出) 및 침출액(浸出液)에서 유리질산(遊離窒酸) 제거(除去) 연구(硏究))

  • Ahn, Jae-Woo;Seo, Jae-Seong
    • Resources Recycling
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    • v.18 no.5
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    • pp.44-51
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    • 2009
  • Fundamental study has been made on the recovery of copper from the electronic scrap by hydrometallurgical process. Nitric acid was used as a leaching agent to dissolve the metals such as Cu, Sn, Pb, Fe etc. from the crushed electronic scraps. TBP was employed to extract nitric acid from the strong nitric acid leaching solutions and to reclaim nitric acid. From the experimental results, Cu was effectively leached by 3.0-4.0 M nitric acid. And 95% of nitric acid in the leaching solution was extracted by 60% TBP, and 98% of nitric acid was stripped from the loaded organic phase by distilled water and it was possible to reuse as a leaching agent.

The Effects of Endogenously and Exogenously Induced Nitric Oxides on the Nociperception of Rats (내.외인성으로 유도된 Nitric Oxide가 흰쥐의 통각전달에 미치는 효과)

  • 방준석;류정수;신창열;양성준;송현주;박전희;제현동;손의동;허인회
    • YAKHAK HOEJI
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    • v.45 no.1
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    • pp.116-124
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    • 2001
  • Nitric oxide is a labile, gaseous, broad spectrum second messenger that used in various tissues and cells. If it is induced by endogenously and exogenously in the neuronal cells, it is able to mediate analgesia or hyperalgesia at the periphery and in the spinal level respectively. This dual role of nitric oxide in the sensory system is very intriguing but has not been fully understood yet. In this experiment, acetylcholine (300 $\mu$g/paw), sodium nitroprusside (600 $\mu$g/paw), and L-arginine (300 $\mu$g/paw) represented antinociceptive effect to noxious topical stimulus, but pronociceptive responses followed by spinally application (20$\mu$g/5$\mu$l, 10$\mu$g/3$\mu$l, 500$\mu$g/5$\mu$l respectively). Calcium ion is critical element which activates nitric oxide synthase, therefore verapamil (300 $\mu$g/paw) and NOS inhibitor (20 mg/kg, L-NAME or L-NOArg) are injected into right hind paw (i.pl.). When verapamil is combined with NOS inhibitors analgesic effects through NO-cGMP pathway are inhibited as compared with ACh alone. Diluted formalin (2.5%), when injected into rats'hind paw (0.05 ml), elicited a biphasic algesic responses and nitric oxide had an analgesic effect on both $A\delta$ and C sensory nerve fibers which manipulate the phases respective1y. Nitric oxides, which produced from constitutive nitric oxide synthase, activated cyclooxygenase-type I and then prostaglandins are produced from them. So, indomethacin and ibuprofen, inhibitors of COX$_1$enzyme, when pretreated intraperitoneally (100 mg/kg) could reduce the hyperalgesic state. From these results, it is possible to imagine that the intrathecally administered NO donors expressed hyperalgesia through both long-term potentiation mechanism and arachidonic acid-prostaglandin cascade.

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Effect of Sacchromyces cerevisiae-Fermented Artemisiae Argi Folium on Nitric oxide Production of Macrophage Treated with Toxicants

  • Park, Wan-Su
    • Journal of Physiology & Pathology in Korean Medicine
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    • v.23 no.4
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    • pp.883-887
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    • 2009
  • The effects of Sacchromyces cerevisiae-Fermented Artemisiae Argi Folium Water extract (AFS) on Nitric oxide production from mouse macrophage Raw 264.7 cells treated with EtOH, gallic acid, Nicotine, Acetaminophen, and Acetaldehyde were investigated through this study. AFS (0, 10, 50, 100, 200, 400 ug/mL) was simultaneously treated with EtOH (100 uM), gallic acid (100 uM), Nicotine (1 mM), Acetaminophen (2 mM), and Acetaldehyde (200 uM). And Nitric oxide production from Raw 264.7 cells was measured by Griess reagent method. AFS restorated the cellular production of Nitric oxide reduced by EtOH, gallic acid, Nicotine, and Acetaminophen in Raw 264.7 cells. AFS could be supposed to have the immuno-modulating activity concerned with macrophage's production of Nitric oxide.