• Tuberculosis and Respiratory Diseases
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• v.43 no.3
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• pp.420-433
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• 1996

Background : There have been many debates about the effects of nitric oxide on the neurogenic inflammation. The role of nitric oxide in the neurogenic inflammation of airways will be required a better understanding of the localization and types of nitirc oxide synthase(NOS) activity in the neurogenic inflammation of airways. Method : To investigate the role of nitric oxide in airway neurogenic inflammation, 1) the effects of neurokinin receptor antagonist (FK224) and nitric oxide synthase inhibitor, $N^{\omega}$-nitro-L-arginine (L-NNA) on plasma extravastion were evaluated in four groups of Sprague-Dawley rats ; sham operation group(sham NANC group), electrical vagal stimulation group(NANC2 group), intravenous pretreatment groups with FK224 (1mg/kg ; FK224 group), and L-NNA(1mg/kg ; L-NNA group) 15 minutes before vagal NANC stimulation. 2) NOS activity in trachea with neurogenic inflammation was localized by immunohistochemical stain. Immunohistochemical stain was performed by antibodies specific for inflammatory cells(iNOS), brain(bNOS), and endothelium (eNOS) on trachea obtained from sham NANC, NANC2, and FK224 groups. Results : The results are that plasma extravsation in neurogenic inflammation of rat airways was inhibited by FK224, but enhanced by L-NNA pretreatment(P<0.05). There was significantly increased infiltration of inflammatory cells in subepithelium of neurogenic inflammatory trachea, but the reduction of subepithelial infiltration of inflammatory cells was observed after pretreatment with FK224(P<0.05). Immunostaining with anti-iNOS antibody showed strong reactivity only in infiltrated inflammatory cells in neurogenic rat trachea, and these iNOS reactivity was reduced by pretreatment with FK224. bNOS immunoreactivity was significantly increased only in the nerves both of neurogenic inflammatory and FK224 pretreated trachea compared with sham NANC trachea(p<0.05). eNOS immunoreactivity was not significant change in endothelium in neurogenic inflammation of rat trachea. Conclusion : These results suggest that nitric oxide released from iNOS in infiltrated inflammatory cells has main role in neurogenic inflammation of rat trachea. The presence of bNOS immunoreactivity in the nerves indicates that nitric oxide may be released from the nerves in rat trachea with neurogenic inflammation.

• Journal of Physiology & Pathology in Korean Medicine
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• v.16 no.1
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• pp.72-77
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• 2002

The present study was examined the effects of Bojungchiseup-tang water extract on the renal expression of renal function regulatory proteins including aquaporin 2 (AQP 2), aquaporin 3 (AQP 3), Na, K-ATPase α1 subunit, endothelial nitric oxide synthase (ecNOS), and inducible nitric oxide synthase (iNOS) in rats. The renal expression of AQP 3 was attenuated in rats administered with Bojungchiseup-tang water extract without altered expression of AQP 2, while ecNOS was up-regualted. Oral administration of Bojungchiseup-tang water extract (40 ㎕/100 g) also attenuated the renal expression of Na, K-ATPase α1-subunit and iNOS protein. These results suggest that the diuretic and natriuretic effects of Bojungchiseup-tang maybe causely related with a decreased expression of AQP 3 and increased expression of ecNOS.

• Korean Journal of Veterinary Research
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• v.41 no.3
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• pp.269-273
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• 2001

The expression of protein kinase C(PKC) isoforms and nitric oxide synthase (NOs) isoforms was studied in the equine vomeronasal organ(VNO), a pheromone receptor organ, using immunohistochemistry. All PKC isoforms including PKC $\alpha$, ${\beta}I$, $\delta$, and $\theta$ were detected in the supporting cells, sensory receptor cells, and basal sensory epithelial cells, while constitutive PKC $\alpha$ and ${\beta}I$ were stained more intensely than novel PKC $\delta$ and ${\theta}$. There was also a varying degree of immunostaining for PKCs in the glandular acini and VNO nerve. Constitutive neuronal and endothelial NOSs, and inducible NOS were detected in the VNO sensory epithelia. There was intense immunoreactivity for endothelial NOS in the VNO sensory epithelia but weak reactivity for neuronal NOS, while inducible NOS showed little immunoreactivity in the adjacent section. These findings suggest that both PKCs and NOSs may be involved in the process of pheromone reception in the horse. Constitutive isoforms of these enzymes may play a more important role in signal trasduction in the VNO of the horse.

• Proceedings of the Korean Society of Toxicology Conference
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• 2002.11b
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• pp.188-189
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• 2002

This work aimed to identify neuronal cell toxicity induced by decrease of physiological NO production by differential phosphorylation of constitutive neuronal NO synthase (nNOS), which can be mediated by Ca2+-dependent PKC and/or CaM-KII activities activated by metals.(omitted)

• Proceedings of the PSK Conference
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• 2003.04a
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• pp.171.1-171.1
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• 2003

In some tissues 17b-estradiol (E2) is known to increase endothelial NOS expression. In the present study we examined the effects of E2 on estrogen receptors (ERa and b) and inducible nitric oxide synthase (iNOS) expression and analyzed the mechanisms in rat peritoneal macrophages. (omitted)

• The Korean Journal of Physiology and Pharmacology
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• v.8 no.3
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• pp.161-165
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• 2004

Exogenous carbon monoxide (0.2%) increases L-type calcium $(Ca^{2+})$ current in human jejunal circular smooth muscle cells. The stimulatory effect of carbon monoxide (CO) on L-type $Ca^{2+}$ current is inhibited by pre-application of L-NNA, a classical competitive inhibitor of nitric oxide synthase (NOS) with no significant isoform selectivity (Lim, 2003). In the present study, we investigated which isoform of NOS affected CO induced stimulation of L-type $Ca^{2+}$ current in human jejunal circular smooth muscle cells. Cells were voltage clamped by whole-cell mode patch clamp technique, and membrane currents were recorded with 10 mM barium as the charge carrier. Before the addition of CO, cells were pretreated with each inhibitor of three NOS isoforms for 15 minutes. CO-stimulating effect on L-type $Ca^{2+}$ current was partially blocked by N-(3-(Amino-methyl) benzyl) acetamidine 2HCl (1400W, an iNOS inhibitor). On the other hand, 3-bromo-7-nitroindazole (BNI, a nNOS inhibitor) or $N^5-(1-Iminoethyl)-L-ornithine$ dihydrochloride (L-NIO, an eNOS inhibitor) completely blocked the CO effect. These data suggest that low dose of exogenous CO may stimulate all NOS isoforms to increase L-type $Ca^{2+}$ channel through nitric oxide (NO) pathway in human jejunal circular smooth muscle cells.

• Asian-Australasian Journal of Animal Sciences
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• v.18 no.5
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• pp.626-631
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• 2005

Nitric oxide (NO) derived from inducible nitric oxide synthase (iNOS) is involved in cell apoptosis, which contributes to luteal regression and luteolysis in some species. In large domestic animals, no direct evidence for the relationship between NO and cell apoptosis in the process of corpus luteum regression is reported. The present study was conducted to investigate the localization of iNOS on porcine corpora lutea (CL) during the oestrus cycle and its relation to cell DNA fragmentation and CL regression. According to morphology, four luteal phases throughout the estrous cycle were defined as CL1, CL2, CL3 and CL4. By isoform-specific antibody against iNOS, the immunochemial staining was determined. Luteal cell DNA fragmentation was determined by flow cytometry. The results showed that no positive staining for iNOS was in CL1 and that iNOS was produced but limited to the periphery of CL2, while in the CL3, the spreading immunochemical staining was found inside the CL. No iNOS positive staining was detected in CL4. Meanwhile, DNA fragmentation increased dramatically when CL developed from CL2 to CL3 (p<0.05). In CL4, higher proportion of luteal cells still had fragmented DNA than that of luteal cells from CL1 or CL2 (p<0.05). These results indicate that iNOS expression is closely related to luteal cell apoptosis and then to luteal regression.

• Korean Journal of Head & Neck Oncology
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• v.17 no.2
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• pp.155-161
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• 2001

Background and Objectives: Nitric oxide (NO) is generated in mammalian tissue by the conversion of L-arginine to L-citrulline. This reaction is catalyzed by nitric oxide synthase (NOS). NO is an important bioactive agent and a signalling molecule that mediates a variety of biologic actions such as vasodilation, neurotransmission, host defense, and iron metabolism but increased NO production may also contribute to the pathogenesis of a various of disorders, including cancer. Before now, the role of NO in thyroid gland is still investigated and it was supposed that NO mediate the angiogenesis in tumor growth. Others journal and works identified the expression of iNOS that involve by neutrophil and eNOS that involve in part in the vascular remodeling and to understand the role of NO in human thyroid gland. But authors revealed only eNOS in thyroid neoplasm. iNOS was identifed by inflammation in fault. Materials and Methods: Western blot analysis was performed, using a polyclonal antibody against eNOS (Rabbit polyclonal IgG). Using the same antibody, the distribution of eNOS was examined in 15 formalin-fixed paraffin embedded samples by immunohistochemistry. By NADPH consumption rate, NOS activity was estimated at nodular hyperplasia. Results: Western blot analysis exhibited that eNOS was significantly elevated in thyroid papillary carcinoma, compared to that in nodular hyperplasia and normal tissue. Immunohistochemistry showed that the immunoreacitivity was present more significantly in thyroid follicular epithelial cell layer than vascular endothelial cell. NOS activity increased in nodular hyperplasia. Conclusions: Thyroid papillary cancer without neutrophil invasion expressed only eNOS. The endothelial localization of eNOS may play an important role in pathogenensis of human thyroid nodular hyperplasia and the follicular localization of thyroid papillary carcinomas.

• Proceedings of the Korean Society of Toxicology Conference
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• 2001.10a
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• pp.131-131
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• 2001

Prostaglandins and nitric oxide produced by inducible cyclooygenase (COX-2) and nitric oxide synthase (iNOS), respectively, have been implicated as important mediators in the process of inflammation and carcinogenesis. On this line, the potential COX-2 or iNOS inhibitors have been considered as anti-inflammatory and cancer chemopreventive agents.(omitted)

• Preventive Nutrition and Food Science
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• v.13 no.4
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• pp.362-365
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• 2008

Agaricus bisporus, also known as white button mushroom, is one of the most popular mushrooms consumed in Korea. This mushroom contains high concentrations of flavanoids and exhibits antioxidant activity. In this study, we examined the effects of Agaricus bisporus ethanol extract (ABE) on lipopolysaccharide (LPS)-induced inflammation in RAW 264.7 cells. Nitric oxide (NO) production and inducible nitric oxide synthase (iNOS) protein levels were assessed in cells treated with $100\;{\mu}M$ LPS in the presence or absence of ABE. 0.5 mg/mL of ABE suppressed NO production significantly. Moreover, ABE inhibited levels of iNOS protein. Taken together, these results suggest that ABE exerts anti-inflammatory activity in LPS-induced inflammation in RAW 264.7 cells.