• Korean Journal of Veterinary Research
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• v.43 no.4
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• pp.551-554
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• 2003

Nitric oxide synthase (NOS) has been reported in uterus. We examined the expression of the NOS isoforms, constitutive endothelial (eNOS) and inducible NOS (iNOS), in bovine uterus by immunohistochemistry. eNOS immunoreactivity was localized predominantly to the endothelial cells that line uterine microvessels and to endometrial glandular epithelial cells, but was barely detectable in endometrial stromal cells. iNOS immunostaining was detected in glandular epithelial and stromal cells in the endometrium and in the endothelial cells of myometrial blood vessels. These findings suggest that both eNOS and iNOS may play important roles in the physiology of the uterus, possibly by generating NO.

• KSBB Journal
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• v.26 no.2
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• pp.172-176
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• 2011

This study was aimed to verify suppressive effect of pine-needle extract on lipopolysaccharide (LPS)-induced inducible nitric oxide synthase (iNOS) expression. In order to evaluate suppressive effect on iNOS expression, RAW 264.7 cells were stably transfected using an iNOS promoterluciferase reporter plasmid yielding RAW 264.7/pGL2-NeomiNOS_ pro11 cells. Established in vitro detection system revealed to diminish LPS-induced iNOS expression by 0.1~500 ${\mu}g/mL$ of saponin at the concentration-dependant manner. Pine needle extract also diminished LPS-induced iNOS expression to 92 and 88% at 500 and 50 ${\mu}g/mL$, respectively. These results suggest that the in vitro detection system developed here could be useful for the verification of suppressive materials on iNOS expression and pine needle extract could be used for the development of functional foods.

• Toxicological Research
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• v.21 no.4
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• pp.285-290
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• 2005

We demonstrate that radicicol, a macrocyclic antifungal antibiotic originally isolated from Monosporium bonorden, inhibits LPS-induced expression of iNOS gene in RAW 264.7 cells. Treatment of peritoneal macrophages and RAW 264.7 cells with radicicol inhibited LPS-stimulated nitric oxide production in a dose-related manner. Immunohistochemical staining of iNOS and RTPCR analysis showed that the decrease of NO was due to the inhibition of iNOS gene expression in RAW 264.7 cells. Immunostaining of p65, EMSA, and reporter gene assay showed that radicicol inhibited $NF-\kappa/Rel$ nuclear translocation. DNA binding, and transcriptional activation, respectively. Collectively, these series of experiments indicate that radicicol inhibits iNOS gene expression by blocking $NF-\kappa/Rel$ nuclear translocation. Due to the critical role that NO release plays in mediating inflammatory responses, the inhibitory effects of radicicol on iNOS suggest that radicicol may represent a useful anti-inflammatory agent.

• Journal of Chest Surgery
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• v.32 no.2
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• pp.138-143
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• 1999

Background: The endothelium-dependent vasorelaxation has been largely accounted for by the release of nitric oxide (NO). Three distinct isoforms of NO synthases (NOS) have been characterized, i.e., brain(bNOS), inducible (iNOS), and endothelial constitutive (ecNOS). Although hypertension hasbeen associated with a vascular endothelial dysfunction, changes in the vascular expression of NOS isoforms have not been established. The present study was aimed at exploring the vascular expression of NOS isozymes in hypertension. Material and Method: Two-kidney, one clip (2K1C) and deoxycorticosterone acetate (DOCA)-salt hypertension were induced in rats. The expression of different NOS isozymes in the thoracic aorta was determined by Western blot analysis. The vascular tissue contents of nitrites were measured by colorimetric assay. Result: Arterial blood pressure was significantly higher in experimental groups of 2K1C and DOCA-salt rats compared with their corresponding control rats. The vascular expression of bNOS as well as that of ecNOS was decreased in both models of hypertension. iNOS was not changed in DOCA-salt hypertension, but was also decreased in 2K1C hypertension. The vascular contents of nitrites were significantly decreased in DOCA-salt as well as in 2K1C hypertension. Conclusion: These results suggest that 2K1C and DOCA-salt hypertension are associated with decreases in the vascular expression of NOS isozymes and nitrite contents.

• The Korean Journal of Physiology and Pharmacology
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• v.13 no.4
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• pp.265-271
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• 2009

Nitric oxide (NO) has both neuroprotective and neurotoxic effects depending on its concentration and the experimental model. We tested the effects of NG-nitro-L-arginine methyl ester (L-NAME), a nonselective nitric oxide synthase (NOS) inhibitor, and aminoguanidine, a selective inducible NOS (iNOS) inhibitor, on kainic acid (KA)-induced seizures and hippocampal CA3 neuronal death. L-NAME (50 mg/kg, i.p.) and/or aminoguanidine (200 mg/kg, i.p.) were administered 1 h prior to the intracerebroventricular (i.c.v.) injection of KA. Pretreatment with L-NAME significantly increased KA-induced CA3 neuronal death, iNOS expression, and activation of microglia. However, pretreatment with aminoguanidine significantly suppressed both the KA-induced and L-NAME-aggravated hippocampal CA3 neuronal death with concomitant decreases in iNOS expression and microglial activation. The protective effect of aminoguanidine was maintained for up to 2 weeks. Furthermore, iNOS knockout mice ($iNOS^{-1-}$) were resistant to KA-induced neuronal death. The present study demonstrates that aminoguanidine attenuates KA-induced neuronal death, whereas L-NAME aggravates neuronal death, in the CA3 region of the hippocampus, suggesting that NOS isoforms play different roles in KA-induced excitotoxicity.

• Asian-Australasian Journal of Animal Sciences
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• v.22 no.7
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• pp.1048-1053
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• 2009

The present study was conducted to determine the effects of chitosan on nitric oxide (NO) content and inducible nitric oxide synthase (iNOS) activity in serum, and relative expression of iNOS mRNA in the duodenum, jejunum, and ileum of broiler chickens. A total of 240 one-day-old Arbor Acre mixed-sex broiler chickens were randomly allotted to six dietary treatments with five replicates in each treatment and eight chickens in each replicate. The broiler chickens in the six treatments were fed the basal diet supplemented with 0 (control), 0.05, 0.2, 0.5, 1.0 or 2.0 g/kg chitosan. The trial lasted for 42 days. The results showed that dietary chitosan enhanced NO content and iNOS activity in serum as well as iNOS mRNA expression in the duodenum and ileum of broiler chickens in a quadratic dose-dependent manner (p<0.05), and improved jejunum iNOS mRNA expression in a quadratic dose-dependent manner (p<0.10) with increasing addition of chitosan. Chicks fed a diet containing 0.5-1.0 g/kg chitosan had higher NO content and iNOS activity in serum as well as small-intestinal iNOS mRNA expression compared with birds given the control diet, but positive effects of chitosan tended to be suppressed when addition of chitosan in the diet was increased to 2.0 g/kg. These results implied that there was a threshold level of chitosan inclusion beyond which progressive reductions in serum NO content and small intestinal iNOS expression occured, and the regulation of chitosan on immune functions in chickens is probably associated with activated expression of iNOS and NO secretion.

• Herbal Formula Science
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• v.15 no.1
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• pp.199-211
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• 2007

Inducible nitric oxide synthase (iNOS) are important inflammation enzyme and severe up-nitric oxide (NO) production by this enzyme has been intricated with pathogenesis of inflammation diseases as atopy dermatitis. The present study was designed in order to determine whether Sopungdojeok-san could inhibit atopy dermatitis through modulation of iNOS mRNA expression and NO production, We found that iNOS mRNA expression and NO production in RAW 264.7 macrophages stimulated with lipopolysaccharide dose-dependantly decreased by Sopungdojeok-san extract treatment (0.4 - 1.0 mg/ml). The distribution of iNOS positive reacted cell in atopy dermatitis elicited skin of mice were remarkably decreased by Sopungdojeok-san administration (2.5 ml/kg/day). The SOD ability of Sopungdojeok-san were dose-dependantly increased from 0.6 mg/ ml than butylated hydroxyanisole. These data likely indicate that Sopungdojeok-san may act as inflammatory regulator for atopy dermatitis may be possible to develop useful agent for chemopreventation of NO-intricate inflammatory diseases.

• Journal of Physiology & Pathology in Korean Medicine
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• v.21 no.5
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• pp.1092-1098
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• 2007

Inducible nitric oxide synthase (iNOS) are important inflammation enzyme and severe up-nitric oxide (NO) production by this enzyme has been intricate with pathogenesis of atopy dermatitis. The present study was designed in order to determine whether Cheonggi-san could inhibit atopy dermatitis through modulation of iNOS mRNA expression and NO production. We found that iNOS mRNA expression and NO production in RAW 264.7 macrophages stimulated with lipopolysaccharide dose-dependantly decreased by Cheonggi-san extract treatment (0.5 - 2.0 mg/ml). The distribution of iNOS positive reacted cell in NC/Nga mice with atopy dermatitis were decreased by Cheonggi-san extract treatment (2.5 ml/kg/day) and apoptosis were increased. These data likely indicate that Cheonggi-san may act as inflammatory regulator for atopy dermatitis and may be possible to develop useful agent for chemoprevention of NO intricate inflammatory diseases.

• THE JOURNAL OF KOREAN ORIENTAL ONCOLOGY
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• v.5 no.1
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• pp.137-150
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• 1999

Macrophage play a major role in host defence against infection and tumor development and this activity is regulated through the production of several mediators. In particular, the production of NO by macrophages mediates killing or growth inhibition of tumor cells, bacteria, fungi and parasites. However, over-expression of iNOS by various stimuli, resulting in over-production of NO, contributes to the pathogenesis of septic shock and some inflammator and auto-immune disease. Therefore, it would be valuable to develop potent and selective inhibitors of for potential therapeutic use. Thus the agent that supprees the expression of iNOS mRNA or enzyme protein will be usefull for the prevention of various diseases. We are intersted in identifying selective inhibitiors of iNOS which might be useful intreating inflammatory human diseases. In summary, we have demenstrated that scopoletin, isolated from Seman Armenicae and Radix Trichosanthis the production of NO induced by $IFN-\gammer$ plus LPS in RAW 264.7 macrophages, The mechanism for the inhibition of NO production was due to suppression of the expression of iNOS mRNA or enzyme protein.

• The Journal of Korean Physical Therapy
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• v.22 no.3
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• pp.71-77
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• 2010

Purpose: To determine whether upregulation of inducible nitric oxide synthase (iNOS) transcription and translation is related to radicular pain in a model of lumbar disc herniation. Also, to investigate the temporal changes of mRNA expression of iNOS and the identity of iNOS and transient receptor potential vanilloid (TRPV) 1 channel expression cells in dorsal root ganglion (DRG) of a model of lumbar disc herniation. Methods: A lumbar disc herniated rat model was developed by implantation of the autologous nucleus pulposus, harvested from the coccygeal vertebra of each tail, on the left L5 nerve root just proximal to the DRG. Rats were tested for mechanical allodynia of the plantar surface of both hind paws 2 days before surgery and 1, 5, 10, 20 and 30 days postoperatively. Reverse transcription polymerase chain reaction (RT-PCR) was used to follow iNOS mRNA expression. To stain iNOS and TRPV1 in DRG, an immunohistochemical study was done 10 days after surgery. Results: A significant drop in mechanical withdrawal threshold on the ipsilateral and contralateral hind paws was observed 1 day after surgery and was prolonged to 30 days in rats with lumbar disc herniation. The expression of mRNA for iNOS peaked at postoperative day 10 on both sides of the DRG. iNOS-positive sensory neurons in the DRG varied in size from large to small diameter cells. A majority of small and intermediate sensory neurons were TRPV1-positive cells. Double immunofluorescence staining for TRPV1 and iNOS revealed that most intermediate TRPV1-positive sensory neurons co-localized with iNOS-positive neurons. Conclusion: Nucleus pulposus-induced mechanical allodynia can be generated without mechanical compression. This pain is related to temporal changes in expression of iNOS mRNA in the DRG. Co-localization of TRPV1 and iNOS in intermediate neurons of the DRG is correlated with pain modality and intensity.