Antiinflammatory effects of mercaptoethylguanidine , a combined inhibitor of nitric oxide synthase and peroxynitrite scavenger , in carrageenan induced models … (1998 Feb)
antiinflammatory effects of mercaptoethylguanidine , a combined inhibitor of nitric oxide synthase and peroxynitrite scavenger , in carrageenan induced models of inflammation . In vitro studies have demonstrated that mercaptoethylguanidine ( MEG ) , a selective inhibitor of the inducible NO synthase ( iNOS ) , is also effective as a scavenger of peroxynitrite ( a potent cytotoxic oxidant produced by the reaction of NO and superoxide ) . In the present study , we evaluated the antiinflammatory potential of MEG treatment in two models of acute inflammation ( carrageenan induced paw edema and pleurisy ) , where oxyradicals , NO , and peroxynitrite play a crucial role in the inflammatory process . Our data show that MEG ( given at 25 microg / paw in the paw edema model or 10 mg / kg in the pleurisy model ) inhibits the inflammatory response ( paw swelling , pleural exudate formation , mononuclear cell infiltration , histological injury ) in both models . furthermore , MEG reduced nitrite / nitrate concentrations in the exudate and reduced the activity of the inducible isoform of NO synthase in the lung ex vivo . MEG also reduced the appearance of nitrotyrosine immunoreactivity in the inflamed tissues . taken together , the present results demonstrate that MEG exerts potent antiinflammatory effects . Part of these antiinflammatory effects may be related to an inhibition of the expression / activity of the inducible NO synthase , another part may be related to oxyradical and peroxynitrite scavenging …

Polyacetylenes from angelica gigas and their inhibitory activity on nitric oxide synthesis in activated macrophages. (2000 Nov)
polyacetylenes from angelica gigas and their inhibitory activity on nitric oxide synthesis in activated macrophages . In activated macrophages the inducible form of nitric oxide synthase ( i NOS ) generates high amounts of the toxic mediator , nitric oxide ( NO ) which contributes to the circulatory failure associated with septic shock . Two polyacetylenes were isolated from the medicinal plant angelica gigas and their structures were elucidated as octadeca 1 , 9 dien 4 , 6 diyn 3 , 8 , 18 triol ( 1 ) and 18 acetoxy octadeca 1 , 9 dien 4 , 6 diyn 3 , 8 diol ( 2 ) by spectroscopic method . these polyacetylenes and their peracetate , 3 , 8 , 18 triacetoxy octadeca 1 , 9 dien 4 , 6 diyn ( 3 ) inhibited the production of NO in LPS activated RAW 264 . 7 cells by suppressing the i NOS enzyme expression . these new inhibitors of i NOS expression may have potential in the treatment of endotoxemia and inflammation accompanied by the overproduction of NO .

Role of nitric oxide in zymosan induced paw inflammation and thermal hyperalgesia. (2001 Apr)
Role of nitric oxide in zymosan induced paw inflammation and thermal hyperalgesia . objective : To assess the involvement of spinal inducible nitric oxide synthase ( iNOS ) in inflammation and nociception . materials AND methods : The time course of iNOS mRNA expression in rat spinal cord and inflamed paw was assessed by means of quantitative real time RT PCR . In addition , the effects of the iNOS inhibitor L NIL on inflammatory paw edema and thermal hyperalgesia were studied in comparison to those of the NO donor RE 2047 . L NIL ( 3 , 9 , 27 and 81 mg / kg ) and RE 2047 ( 3 , 9 and 27 mg / kg ) or vehicle were administered orally 15 min prior to the intraplantar injection of 0 . 625 mg zymosan . results : following zymosan injection , mRNA expression of iNOS increased in the inflamed paw and spinal cord with a maximum at 2 . 5 and 4 h , respectively . In the spinal cord iNOS mRNA started to decline at 10 h whereas it remained at maximum in the inflamed paw up to the end of the observation period of 24 h . As expected , RE 2047 had significant pronociceptive and proinflammatory effects . L NIL significantly reduced paw inflammation at 27 and 81 mg / kg but failed to reduce hyperalgesia at the doses tested . conclusions : The results show that iNOS is upregulated in the inflamed …

Oxidative stress related molecules as a therapeutic target for inflammatory and allergic diseases. (2005 Aug)
oxidative stress related molecules as a therapeutic target for inflammatory and allergic diseases . there is a growing body of evidence that oxidative stress mediated by reactive oxygen species plays an important role in the pathogenesis of various kinds of allergic and non allergic inflammation . these data suggest that blocking reactive oxygen species should be useful for amelioration of allergic or non allergic inflammation in the respiratory and intestinal tracts . In addition , the modulation of oxidative stress related molecules , such as inducible nitric oxide synthase and redox sensitive transcriptional factors , may be useful for the regulation of these inflammatory responses . In this review , we have summarized the recent advances in the prevention of allergic or non allergic inflammation , especially the diesel exhaust particle induced respiratory allergic response and dextran sulfate sodium induced intestinal inflammation in rodents .

Exhaled nitric oxide ( NO ) in patients with respiratory tract diseases nitric oxide ( NO ) is highly active … (2004 Jun)
exhaled nitric oxide ( NO ) in patients with respiratory tract diseases nitric oxide ( NO ) is highly active molecule playing a key role in physiological as well as in pathological processes in the organism . asthmatic patients show an increased expression of inducible nitric oxide synthase ( iNOS ) in airway epithelial cells and an increased level of NO in exhaled air . The aim of the study was to evaluate the exhaled NO in different groups of allergic patients and healthy volunteers . The study was conducted in the group of 94 patients and healthy subjects . NO was measured in exhaled air by means of chemiluminescence ( model 280 nitric oxide analyzer . sievers instruments , Inc , USA . healthy , nonsmoking subjects had exhaled NO levels of 10 20 ppB and smoking was one of the factors reduces exhaled NO . exhaled NO was elevated in asthma patients . The patients with stable COPD have been shown to have exhaled NO on the same level that healthy smoking subjects . We observed , that the study patients with pollinosis who did not have asthma symptoms had increased levels of exhaled NO during pollen season . measurement of exhaled NO is an easy , non invasive procedure that can be used to monitor the level of airway inflammation .

Effect of leaf extract of seabuckthorn on lipopolysaccharide induced inflammatory response in murine macrophages. (2005 Dec)
effect of leaf extract of seabuckthorn on lipopolysaccharide induced inflammatory response in murine macrophages . nitric oxide ( NO ) is synthesized in large quantities by activated inflammatory cells and has been demonstrated to be involved in the pathogenesis of acute and chronic inflammatory conditions . seabuckthorn ( SBT ) has been used in traditional medicine systems for the treatment of various diseases like cardiovascular , pain relief , oral inflammation and promotion of tissue regeneration . The present study focuses on the effects of SBT leaf extract on NO production induced by lipopolysaccharide ( LPS ) in the murine macrophage cell line RAW 264 . 7 . In addition , cell viability , free radical scavenging activity and inducible nitric oxide synthase ( iNOS ) expression were also evaluated . seabuckthorn leaf extract significantly inhibited the enhanced production of NO induced by LPS in a dose dependent manner . treatment with SBT did not reduce cell viability at any dose used . The extract showed significant scavenging of NO radicals released by the NO donor . treatment of macrophages with SBT leaf extract also caused a significant inhibition of iNOS activation . these observations suggest that the inhibition of net NO production by SBT leaf extract may be due to its scavenging activity and / or its inhibitory effects on iNOS activation . The study suggests that SBT leaf extract has significant anti inflammatory activity and has potential for the treatment of inflammatory diseases .

Nitric oxide synthase II is expressed in severe corneal alkali burns and inhibits neovascularization. (1999 Nov)
nitric oxide synthase II is expressed in severe corneal alkali burns and inhibits neovascularization . purpose : inducible nitric oxide synthase ( NOS II ) is expressed in many inflammatory conditions . The implication of nitric oxide ( NO ) in angiogenesis remains controversial . The role of NOS II and its influence on angiogenesis in corneal neovascularization is unknown and was investigated in this study . methods : A mouse model of corneal neovascularization induced by chemical cauterization was used . NOS II mRNA expression was analyzed by reverse transcriptase polymerase chain reaction , and NOS II protein was studied in situ by immunohistochemical analysis of the cornea . The influence of NOS II on neovascularization was determined by comparison of vessel development in normal wild type mice and mice with a targeted disruption of the NOS II gene . results : NOS II mRNA was induced to very high levels after corneal cauterization and remained upregulated throughout the disease . migratory cells in the center of the cauterization area expressed NOS II protein . The neovascular response in mice lacking the NOS II gene was significantly stronger than in wild type mice , and the difference increased over time . conclusions : these data are the first evidence that NOS II is expressed in this model of sterile corneal inflammation . NOS II expression inhibited angiogenesis in severe corneal alkali burns .

Lovastatin reduces apoptosis and downregulates the CD40 expression induced by TNF alpha in cerebral vascular endothelial cells. (2006 Feb)
lovastatin reduces apoptosis and downregulates the CD40 expression induced by TNF alpha in cerebral vascular endothelial cells . inflammation may be one of the independent risk factors contributing to many neurological diseases . moreover , there is an emerging body of data indicating that statins may have neuroprotective action . recent studies suggest that CD40 CD40 ligand ( cd40l ) system is proven to be an important mediator of several auto immune and chronic inflammation diseases . To address whether lovastatin produces neuroprotection as a potential novel anti inflammatory pathway through the inhibition of CD40 expression , we examined the possible effects of lovastatin on expression of CD40 , apoptosis , level of nitric oxide ( NO ) and nitric oxide synthase ( NOS ) activity induced by tumor necrosis factor alpha ( TNF alpha ) in the cerebral vascular endothelial cells ( cvecs ) involved in cerebrovascular diseases . preincubation with lovastatin ( 10 ( 7 ) , 10 ( 6 ) and 10 ( 5 ) mol / l ) for 24 hours ( h ) protected cvecs from TNF alpha induced decrease of cellular viability . further , lovastatin inhibited the TNF alpha induced increases of NO level , NOS activity , apoptotic cells and CD40 expression in a dose dependent manner , and anti CD40 antibody also inhibited the cellular apoptosis induced by TNF alpha . In conclusion , our data provide evidence to support a direct pro inflammatory effect of CD40 cd40l signaling pathway in …

Mechanisms of homocysteine induced atherothrombosis. (2005 Aug)
mechanisms of homocysteine induced atherothrombosis . elevation of plasma homocysteine level is a risk factor for cardiovascular disease , stroke , and venous thromboembolism . It is still uncertain , however , whether hyperhomocysteinemia is a causative factor or a marker of vascular disease . The strongest evidence that homocysteine plays a causal role in atherothrombosis has been provided by studies using animal models . In the past decade , considerable progress in defining the vascular effects of hyperhomocysteinemia was achieved through the use of genetic and dietary approaches to induce hyperhomocysteinemia in experimental animals . A key vascular phenotype observed in hyperhomocysteinemic animals is endothelial dysfunction , manifested by decreased bioavailability of endothelium derived nitric oxide . impairment of endothelial function may be mediated by either accelerated oxidative inactivation of nitric oxide or inhibition of nitric oxide production caused by the endogenous nitric oxide synthase inhibitor , asymmetric dimethylarginine . hyperhomocysteinemia also increases susceptibility to arterial thrombosis and accelerates the development of atherosclerosis in susceptible models such as the apolipoprotein E deficient mouse . mechanisms of atherothrombosis may include homocysteine induced thiolation or acylation of plasma or endothelial proteins and endoplasmic reticulum stress , which activates signal transduction pathways leading to inflammation and apoptosis .

Hydrogen sulfide attenuates lipopolysaccharide induced inflammation by inhibition of p38 mitogen activated protein kinase in microglia. (2007 Feb)
hydrogen sulfide attenuates lipopolysaccharide induced inflammation by inhibition of p38 mitogen activated protein kinase in microglia . The present study attempts to investigate the effect of H ( 2 ) S on lipopolysaccharide ( LPS ) induced inflammation in both primary cultured microglia and immortalized murine BV 2 microglial cells . We found that exogenous application of sodium hydrosulfide ( NaHS ) ( a H ( 2 ) S donor , 10 300 micro mol / L ) attenuated LPS stimulated nitric oxide ( NO ) in a concentration dependent manner . stimulating endogenous H ( 2 ) S production decreased LPS stimulated NO production , whereas lowering endogenous H ( 2 ) S level increased basal NO production . western blot analysis showed that both exogenous and endogenous H ( 2 ) S significantly attenuated the stimulatory effect of LPS on inducible nitric oxide synthase expression , which is mimicked by SB 203580 , a specific p38 mitogen activated protein kinase ( MAPK ) inhibitor . exogenously applied NaHS significantly attenuated LPS induced p38 MAPK phosphorylation in BV 2 microglial cells . moreover , both NaHS ( 300 micro mol / L ) and SB 203580 ( 1 micro mol / L ) significantly attenuated LPS induced tumor necrosis factor alpha secretion , another inflammatory indicator . In addition , NaHS ( 10 300 micro mol / L ) dose dependently decreased LPS stimulated NO production in primary cultured astrocytes , suggesting that the anti neuroinflammatory effect of H …

Exhaled nitric oxide ( NO ) in asthma patients with acute exacerbation In recent years there has been an upsurge … (2004 Jun)
exhaled nitric oxide ( NO ) in asthma patients with acute exacerbation In recent years there has been an upsurge in interest in exhaled markers of inflammation , and nitric oxide ( NO ) in particular . The aim of the study was to evaluate the exhaled NO in monitoring anti inflammatory therapy in asthma patients with acute exacerbation . The study was conducted in the group of 12 asthma patients , during acute asthma exacerbation treated with oral corticosteroids . NO was measured in exhaled air by means of chemiluminescence ( model 280i nitric oxide analyzer , sievers instruments , Inc , USA . during 15 days of study a significant decrease in exhaled NO was observed . In our study the improvement of this inflammation marker correlated with clinical markers of disease control ( the need for rescue beta 2 agonist use ) . The significant decrease in exhaled NO was started long before than increase in spirometric parameters . treatment of airway inflammation in asthma with systemic and inhaled corticosteroids reduces levels of NO in exhaled air . measurement of exhaled NO is non invasive , safe and causes no inconvenience to the patients method to monitoring of anti inflammatory therapy .

Inducible nitric oxide synthase expression in coronary arteries of transplanted human hearts with accelerated graft arteriosclerosis. (1997 Oct)
inducible nitric oxide synthase expression in coronary arteries of transplanted human hearts with accelerated graft arteriosclerosis . inducible nitric oxide synthase ( iNOS ) is a high output isoform of NOS that produces nitric oxide ( NO ) , a nonspecific immune effector molecule . In some animal models of autoimmunity , the induction of iNOS has been shown to lead to inflammation and tissue damage , and it has been suggested that iNOS is an immune mediator in humans as well . using in situ hybridization and immunohistochemical techniques , we demonstrate that iNOS mRNA and protein are present in the coronary arteries of transplanted human hearts with accelerated graft arteriosclerosis ( AGA ) . iNOS is expressed in cells morphologically consistent with macrophages in the neointima of 7 of 10 of the transplanted vessels with AGA that were examined . In serial sections , these same cells express the macrophage marker CD68 . In contrast , iNOS is absent from five native coronary arteries with atherosclerosis and absent from two normal coronary arteries . although iNOS is expressed in macrophages in AGA , its role in the pathogenesis of AGA is unknown .

Nitric oxide production and signaling in inflammation. (2005 Aug)
nitric oxide production and signaling in inflammation . nitric oxide ( NO ) is recognized as a mediator and regulator of inflammatory responses . It possesses cytotoxic properties that are aimed against pathogenic microbes , but it can also have damaging effects on host tissues . NO reacts with soluble guanylate cyclase to form cyclic guanosine monophosphate ( cGMP ) , which mediates many of the effects of NO . NO can also interact with molecular oxygen and superoxide anion to produce reactive nitrogen species that can modify various cellular functions . these indirect effects of NO have a significant role in inflammation , where NO is produced in high amounts by inducible nitric oxide synthase ( iNOS ) and reactive oxygen species are synthesized by activated inflammatory cells . The present review deals with NO production and signaling in inflammation , especially in relation to human neutrophils and eosinophils .

Expression of inducible nitric oxide synthase ( iNOS ) mRNA in inflamed esophageal and colonic mucosa in a pediatric population. (1998 Jun)
expression of inducible nitric oxide synthase ( iNOS ) mRNA in inflamed esophageal and colonic mucosa in a pediatric population . objective : increasing evidence suggests that nitric oxide participates in the pathophysiology of intestinal barrier function / dysfunction and inflammation . increases in inducible nitric oxide synthase ( iNOS ) mRNA and protein expression have been observed in colonic mucosal biopsies of adults with inflammatory bowel disease ( IBD ) . It is unclear whether iNOS induction is specific for IBD or a reflection of nonspecific mucosal inflammation . furthermore , the characteristics of iNOS mRNA expression in pediatric patients with gastrointestinal disorders remains ill defined . Our objective was to examine the relationship between iNOS mRNA expression and gastrointestinal mucosal inflammation in a pediatric population . methods : esophageal and colonic mucosal biopsies were obtained during endoscopy . total RNA was isolated from these biopsies and reverse transcription polymerase chain reaction ( RT PCR ) performed ( 35 PCR cycles ) using two 20 bp primers that amplified a predicted 372 bp conserved iNOS mRNA fragment . results : biopsies were obtained from 29 children ( 22 boys ; mean age 10 . 6 yr range 1 . 7 16 . 5 yr ) . endoscopic and histological findings included normal esophageal mucosa ( n 3 ) , esophagitis ( n 10 ) , normal rectal mucosa ( n 2 ) , ulcerative colitis ( n 10 ) , and crohn disease ( n 4 ) . evidence …

Cytokines regulate vascular functions related to stability of the atherosclerotic plaque. (1996 Sep)
cytokines regulate vascular functions related to stability of the atherosclerotic plaque . The cytokines are multipotent mediators of inflammation and immunity that can affect key functions of vascular wall cells . growing evidence suggests that cytokines participate as autocrine or paracrine mediators in atherogenesis , as cells in lesions can both produce and respond to these mediators . The functions of vascular wall cells regulated by cytokines may influence lesion initiation , progression , or complication . For example , cytokines can regulate the expression of adhesion molecules crucial to the recruitment of leukocytes to lesions , including vascular cell adhesion molecule 1 ( VCAM 1 ) . cytokines such as interleukin 1 ( IL 1 ) and tumor necrosis factor alpha ( TNF alpha ) can regulate the production of monocyte chemoattractant protein 1 ( MCP 1 ) , a potential signal for directed migration of monocytes into the intima . cytokines can also regulate genes that encode other growth factors and cytokines themselves . TNF alpha can induce IL 1 mRNA in human endothelial ( EC ) and smooth muscle cells ( SMC ) . IL 1 and TNF alpha can augment the production by vascular cells of macrophage colony stimulating factor ( M CSF ) , which may promote growth and activation of mononuclear phagocytes . cytokines can exert both pro and antiatherogenic actions . activated T cells in human atheroma may secrete the lymphokine IFN gamma , an inhibitor of SMC proliferation . cytokines influence vasomotor …

Decreased iNOS synthesis mediates dexamethasone induced protection of neurons from inflammatory injury in vitro. (2003 Nov)
decreased iNOS synthesis mediates dexamethasone induced protection of neurons from inflammatory injury in vitro . brain inflammation is accompanied by transection of axons and death of neurons in the acute lesions of multiple sclerosis . We explored mechanisms of inflammatory damage to neurons in vitro using cocultures of rat embryonal cortical neurons with microglia activated by interferon gamma ( ifngamma ) and lipopolysaccharide ( LPS ) . previously , we have demonstrated that microglia are highly toxic to neurons and that nitric oxide ( NO ) derived from inducible nitric oxide synthase ( iNOS ) is necessary and sufficient to mediate this toxicity . Here , we show that addition of dexamethasone ( 1 micro M ) to activated cocultures provides effective neuroprotection . We demonstrate that dexamethasone down regulates NO production of primary microglia by approximately 50 and reduces steady state iNOS protein and mRNA expression by approximately 70 . these changes were reversed by the glucocorticoid receptor blocker RU 486 . furthermore , we analysed the stability of iNOS protein and show that whilst inhibitors of the proteasome blocked iNOS degradation they did not reverse the dexamethasone effect . Our results indicate that the main mechanism of corticosteroid activity on iNOS is reduction in protein synthesis , not destabilization as previously suggested .

Endotoxin induced nitric oxide production rescues airway growth and maturation in atrophic fetal rat lung explants. (2006 Sep)
endotoxin induced nitric oxide production rescues airway growth and maturation in atrophic fetal rat lung explants . inflammation induces premature maturation of the fetal lung but the signals causing this effect remain unclear . We determined if nitric oxide ( NO ) synthesis , evoked by escherichia coli lipopolysaccharide ( LPS , 2 microg ml 1 ) , participated in this process . fetal rat lung airway surface complexity rose 2 . 5 fold over 96h in response to LPS and was associated with increased iNOS protein expression and activity . iNOS inhibition by N6 ( 1 iminoethyl ) L lysine 2HCl ( L NIL ) abolished this and induced airway atrophy similar to untreated explants . surfactant protein C ( SP C ) expression was also induced by LPS and abolished by L NIL . As tgfbeta suppresses iNOS activity , we determined if feedback regulation modulated NO dependent maturation . LPS induced tgfbeta1 release and smad4 nuclear translocation 96 h after treatment . treatment of explants with a blocking antibody against tgfbeta1 sustained NO production and airway morphogenesis whereas recombinant tgfbeta1 antagonized these effects . feedback regulation of NO synthesis by tgfbeta may , thus , modulate airway branching and maturation of the fetal lung .

Free fatty acid impairment of nitric oxide production in endothelial cells is mediated by ikkbeta. (2005 May)
Free fatty acid impairment of nitric oxide production in endothelial cells is mediated by ikkbeta . objective : Free fatty acids ( FFA ) are commonly elevated in diabetes and obesity and have been shown to impair nitric oxide ( NO ) production by endothelial cells . however , the signaling pathways responsible for FFA impairment of NO production in endothelial cells have not been characterized . insulin receptor substrate 1 ( IRS 1 ) regulation is critical for activation of endothelial nitric oxide synthase ( eNOS ) in response to stimulation by insulin or fluid shear stress . methods AND results : We demonstrate that insulin mediated tyrosine phosphorylation of IRS 1 and serine phosphorylation of Akt , eNOS , and NO production are significantly inhibited by treatment of bovine aortic endothelial cells with 100 micromol / L FFA composed of palmitic acid for 3 hours before stimulation with 100 nM insulin . This FFA preparation also increases , in a dose dependent manner , ikkbeta activity , which regulates activation of NF kappab , a transcriptional factor associated with inflammation . similarly , elevation of other common FFA such as oleic and linoleic acid also induce ikkbeta activation and inhibit insulin mediated eNOS activation . overexpression of a kinase inactive form of ikkbeta blocks the ability of FFA to inhibit insulin dependent NO production , whereas overexpression of wild type ikkbeta recapitulates the effect of FFA on insulin dependent NO production . conclusions : elevated levels of common …

Exhaled nitric oxide in children with asthma and sinusitis. (2007 Sep)
exhaled nitric oxide in children with asthma and sinusitis . exhaled nitric oxide ( FE ( NO ) ) is a surrogate marker of eosinophilic airway inflammation . The measurement of this gas can be easily performed in children and the result is immediately available . because of these characteristics , measurement of FE ( NO ) is slowly becoming part of the routine clinical evaluation of an asthmatic patient . FE ( NO ) measurement may have a role both in the diagnosis of asthma and as a guide in therapy algorithms . For example when FE ( NO ) levels are persistently normal and the asthmatic child is asymptomatic , the steroid therapy may be decreased or even stopped . In patients with acute or chronic rhinosinusitis the levels of nasal nitric oxide ( nNO ) are significantly decreased , while they rise up after a course of antibiotics . The measurement of nasal NO has been proposed as a functional test to evaluate sinus ventilation . nasal NO is significantly reduced also in primary ciliary dyskinesia and can be used as a screening tool to identify patients affected by this condition .

Expression of nitric oxide synthase and its significance in nasal polyps objective : To study the expression of nitric oxide … (2004 Sep)
expression of nitric oxide synthase and its significance in nasal polyps objective : To study the expression of nitric oxide synthase ( NOS ) and its activity in nasal polyps and its significance . method : septectomy and immunohistochemisty were used to examine NOS activity and identify the expression of inducible NOS ( iNOS ) and endotheial NOS ( eNOS ) in human nasal specimens from patients undergoing nasal spectrumtomy ( n 20 ) or nasal polypectomy ( n 30 ) . result : The activity of NOS was significantly higher in nasal polyps than in nasal mucosa ( 4 . 079 / 0 . 655 ) U / Pro vs ( 1 . 526 / 0 . 310 ) U / Pro ( P 0 . 01 ) . iNOS reaction product was located in epithelial cells , vascular endothelial cells , nasal glands and inflammation cells of nasal polyps . iNOS reaction product almost was not be founded in nasal mucosa . amount of . iNOS positive cells in nasal polyps was higher than in nasal mucosa ( P 0 . 01 ) . eNOS reaction product were located in nasal polyps and nasal mucosa . there was no quantitative difference of eNOS between in nasal polyps and nasal mucosa . amount of iNOS positive cells was significantly higher than of eNOS positive cells in nasal polyps ( P 0 . 01 ) . conclusion : iNOS , mainly expressed in nasal polyps , locates in epithelial cells …