Acute pancreatitis is an initially localized inflammation of the pancreatic gland. The precise mechanisms by which aetiological factors induce acute pancreatitis are not yet known, but when initiated, common inflammatory pathways seem to be involved, with cytokines being their components of major importance. The inducible nitric oxide synthase gene (iNOS) encodes an enzyme involved in the pathway of reactive oxygen species and induced in response to infection, cytokines. iNOS is capable of generating large quantities of nitric oxide produced during inflammation. The objective of this study was to investigate the association between acute pancreatitis risk and iNOS polymorphisms. The studied single-nucleotide polymorphisms (SNPs) were Ser608Leu, resulting in an amino acid substitution, and 1173C/T and 954G/C, both in the gene promoter region that is linked to increased enzyme expression, leading to higher NO production. The genotypes for the three SNPs were determined in 93 patients with acute pancreatitis and 60 controls without pancreatitis or cancer that were matched for age and gender. Data analysis was done by conditional logistic regression. It was found that the Ser608Leu polymorphism was more frequent among cases with acute pancreatitis compared to controls (OR = 2.88; 95% CI: 1.49-5.57; P = 0.002), although no individually statistically significant associations for the other SNPs studied were detected. We suggest that iNOS Ser608Leu can be used as a marker to define the risk of acute pancreatitis.

• MeSH
• akutní nemoc MeSH
• frekvence genu genetika   MeSH
• genetická predispozice k nemoci * MeSH
• jednonukleotidový polymorfismus genetika   MeSH
• lidé středního věku MeSH
• lidé MeSH
• pankreatitida enzymologie   genetika   MeSH
• rizikové faktory MeSH
• senioři MeSH
• studie případů a kontrol MeSH
• substituce aminokyselin genetika   MeSH
• synthasa oxidu dusnatého, typ II genetika   MeSH
• Check Tag
• lidé středního věku MeSH
• lidé MeSH
• mužské pohlaví MeSH
• senioři MeSH
• ženské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• NOS2 protein, human MeSH Prohlížeč
• synthasa oxidu dusnatého, typ II MeSH

Pathogenesis of hypoxic pulmonary hypertension is initiated by oxidative injury to the pulmonary vascular wall. Because nitric oxide (NO) can contribute to oxidative stress and because the inducible isoform of NO synthase (iNOS) is often upregulated in association with tissue injury, we hypothesized that iNOS-derived NO participates in the pulmonary vascular wall injury at the onset of hypoxic pulmonary hypertension. An effective and selective dose of an iNOS inhibitor, L-N6-(1-iminoethyl)lysine (L-NIL), for chronic peroral treatment was first determined (8 mg/l in drinking water) by measuring exhaled NO concentration and systemic arterial pressure after LPS injection under ketamine+xylazine anesthesia. A separate batch of rats was then exposed to hypoxia (10% O2) and given L-NIL or a nonselective inhibitor of all NO synthases, N(G)-nitro-L-arginine methyl ester (L-NAME, 500 mg/l), in drinking water. Both inhibitors, applied just before and during 1-wk hypoxia, equally reduced pulmonary arterial pressure (PAP) measured under ketamine+xylazine anesthesia. If hypoxia continued for 2 more wk after L-NIL treatment was discontinued, PAP was still lower than in untreated hypoxic controls. Immunostaining of lung vessels showed negligible iNOS presence in control rats, striking iNOS expression after 4 days of hypoxia, and return of iNOS immunostaining toward normally low levels after 20 days of hypoxia. Lung NO production, measured as NO concentration in exhaled air, was markedly elevated as early as on the first day of hypoxia. We conclude that transient iNOS induction in the pulmonary vascular wall at the beginning of chronic hypoxia participates in the pathogenesis of pulmonary hypertension.

• MeSH
• aplikace orální MeSH
• arteria pulmonalis enzymologie   MeSH
• časové faktory MeSH
• chronická nemoc MeSH
• hypoxie komplikace   enzymologie   metabolismus   patofyziologie   MeSH
• inhibitory enzymů aplikace a dávkování   farmakologie   MeSH
• krysa rodu Rattus MeSH
• lysin aplikace a dávkování   analogy a deriváty   farmakologie   MeSH
• NG-nitroargininmethylester farmakologie   MeSH
• oxid dusnatý MeSH
• plíce metabolismus   MeSH
• plicní hypertenze etiologie   patofyziologie   MeSH
• potkani Wistar MeSH
• synthasa oxidu dusnatého, typ II antagonisté a inhibitory   biosyntéza   MeSH
• tyrosin analogy a deriváty   metabolismus   MeSH
• vydechnutí MeSH
• vztah mezi dávkou a účinkem léčiva MeSH
• zvířata MeSH
• Check Tag
• krysa rodu Rattus MeSH
• mužské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• 3-nitrotyrosine MeSH Prohlížeč
• inhibitory enzymů MeSH
• lysin MeSH
• N(6)-(1-iminoethyl)lysine MeSH Prohlížeč
• NG-nitroargininmethylester MeSH
• oxid dusnatý MeSH
• synthasa oxidu dusnatého, typ II MeSH
• tyrosin MeSH

OBJECTIVE: Nitric oxide is an important vasoactive mediator. Changes in NO production, caused by functional variants of both endothelial and inducible NO synthase (eNOS, iNOS), might play a role in portal hypertension. The aim was to study the significance of functional eNOS and iNOS gene variants in cirrhotic patients and their interrelationship to both inflammatory and endothelial activation parameters. MATERIAL AND METHODS: One hundred and thirty-two patients with liver cirrhosis (age 36-72 years) and 101 controls were examined for functional variants of eNOS (E298D, 27bpintr4, 786T/C) and iNOS (R221W, S608L) genes. Inflammatory (IL6, IL8, IL10) and vasoactive (sVCAM-1, E-selectin) cytokines were measured using ELISA kits. RESULTS: The frequency of E298D (GG 12%, GT 41%, TT 47%), 28bpintr4 (AA 6%, AB 28%, BB 66%), 786T/C genotypes (CC 17%, CT 45%, TT 38%), as well as R221W (CC 93%, CT 7%, TT 0%), and S608L (CC 65%, CT 32%, TT 3%) genotypes in cirrhotic patients did not differ from the controls (p > 0.05 for all comparisons). No relationship was found between the frequency of these genotypes and the severity of portal hypertension, or either inflammatory or vasoactive cytokines. A positive correlation was found between hepatic venous pressure gradient and cytokine concentration: sVCAM-1, IL6, IL8, IL10. CONCLUSIONS: Examined eNOS and iNOS variants have no relationship to pathogenesis of liver cirrhosis. Severity of portal hypertension was associated with the changes in endothelial activation.

• MeSH
• cytokiny krev   MeSH
• DNA primery chemie   MeSH
• dospělí MeSH
• ELISA MeSH
• genetická variace MeSH
• genotyp MeSH
• jaterní cirhóza komplikace   genetika   MeSH
• lidé středního věku MeSH
• lidé MeSH
• polymerázová řetězová reakce metody   MeSH
• portální hypertenze etiologie   genetika   MeSH
• senioři MeSH
• studie případů a kontrol MeSH
• stupeň závažnosti nemoci MeSH
• synthasa oxidu dusnatého, typ II genetika   MeSH
• synthasa oxidu dusnatého, typ III genetika   MeSH
• Check Tag
• dospělí MeSH
• lidé středního věku MeSH
• lidé MeSH
• mužské pohlaví MeSH
• senioři MeSH
• ženské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• cytokiny MeSH
• DNA primery MeSH
• NOS2 protein, human MeSH Prohlížeč
• NOS3 protein, human MeSH Prohlížeč
• synthasa oxidu dusnatého, typ II MeSH
• synthasa oxidu dusnatého, typ III MeSH

The aim of this study was to compare the effectiveness of immunosuppressant FK 506 and the specific inhibitor of inducible nitric oxide synthase (iNOS) aminoguanidine (AG) in prevention of corneal graft rejection and to investigate the iNOS expression in the rejection process. Orthotopic corneal allografting in mice was performed (C57BL/10; H-2(b) to BALB/c; H-2(d)). FK 506 (0.3 mg/kg per day) or AG (100 mg/kg per day) was injected intraperitoneally for 4 weeks. Grafted mice without therapy served as controls. Immunohistological evaluation of iNOS-positive cells and macrophage infiltration in grafts 27th day after grafting was performed. Within 4 weeks FK 506 prevented graft rejection in 71% and AG in 57% of animals compared to 29% of clear grafts in controls. A significant proportion of iNOS-positive cells was detected in the rejected grafts of the control and AG-treated groups. The treatment with FK 506 resulted in the inhibition of iNOS expression to a high degree in the rejected corneas. Non-rejected corneas of all groups and non-transplanted corneas exhibited no iNOS-positive cells. A massive infiltration of macrophages was detected in the rejected grafts, whereas non-rejected grafts exhibited only slight infiltration of macrophages. The presented data suggest that overexpression of iNOS and/or activation of iNOS is one of the several influential factors that contribute to the rejection process and that iNOS suppression delays corneal allograft rejection. FK 506 and AG are effective drugs in preventing corneal allograft rejection. Higher beneficial effect of FK 506 on graft survival could be explained by its well-known selective T-cell immunosuppression.

• MeSH
• guanidiny farmakologie   MeSH
• imunohistochemie MeSH
• imunosupresiva farmakologie   MeSH
• inhibitory enzymů farmakologie   MeSH
• makrofágy účinky léků   imunologie   MeSH
• myši inbrední BALB C MeSH
• myši inbrední C57BL MeSH
• myši MeSH
• přežívání štěpu účinky léků   imunologie   MeSH
• rejekce štěpu enzymologie   imunologie   prevence a kontrola   MeSH
• synthasa oxidu dusnatého, typ II MeSH
• synthasa oxidu dusnatého antagonisté a inhibitory   biosyntéza   MeSH
• takrolimus farmakologie   MeSH
• transplantace rohovky imunologie   MeSH
• zvířata MeSH
• Check Tag
• mužské pohlaví MeSH
• myši MeSH
• ženské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• srovnávací studie MeSH
• Názvy látek
• guanidiny MeSH
• imunosupresiva MeSH
• inhibitory enzymů MeSH
• Nos2 protein, mouse MeSH Prohlížeč
• pimagedine MeSH Prohlížeč
• synthasa oxidu dusnatého, typ II MeSH
• synthasa oxidu dusnatého MeSH
• takrolimus MeSH

The aim of this study was to investigate longitudinal changes of the pulmonary inflammatory process as a result of mechanical stress due to mechanical ventilation. The concentrations of IL-8, TNF-α, MIP-1β, nitrites/nitrates, and inducible nitric oxide synthases (iNOS) were investigated indicate in bronchoalveolar lavage (BAL). Twenty-three piglets were divided into three groups. Group I: animals breathing spontaneously; group II: mechanical ventilation (tidal volume (TV) = 7 mL/kg, PEEP = 5 cmH(2)O); group III: mechanical ventilation (TV = 15 mL/kg, PEEP = 0 cmH(2)0). Concentrations of BAL nitrites/nitrates from groups II and III increased during the first hour of mechanical ventilation (P = .03 and .02, respectively). The highest expression of iNOS was observed during the first hour in groups II and III. IL-8 concentration increased significantly in groups II and III. Production of TNF-α increased significantly in group III during the second and third hour (P = .01). Concentration of MIP-1β was significantly increased in groups II and III after the first hour (P = .012 and P = .008, respectively).

• MeSH
• akutní poškození plic etiologie   metabolismus   MeSH
• bronchoalveolární lavážní tekutina chemie   cytologie   MeSH
• chemokin CCL4 metabolismus   MeSH
• cytokiny metabolismus   MeSH
• dechový objem MeSH
• dusičnany metabolismus   MeSH
• dusitany metabolismus   MeSH
• interleukin-8 metabolismus   MeSH
• plíce metabolismus   patologie   patofyziologie   MeSH
• plicní alveoly metabolismus   patologie   MeSH
• poddajnost plic fyziologie   MeSH
• prasata MeSH
• synthasa oxidu dusnatého, typ II metabolismus   MeSH
• TNF-alfa metabolismus   MeSH
• umělé dýchání škodlivé účinky   MeSH
• ventilace umělá s výdechovým přetlakem přístrojové vybavení   MeSH
• zvířata MeSH
• Check Tag
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• chemokin CCL4 MeSH
• cytokiny MeSH
• dusičnany MeSH
• dusitany MeSH
• interleukin-8 MeSH
• synthasa oxidu dusnatého, typ II MeSH
• TNF-alfa MeSH

Nasal polyps (NP), edematous projections of nasal mucosa (NM), are characterized by an inflammatory cellular infiltrate, however, little is known about etiopathogenesis of NP. Both innate immune mechanisms leading to activation of NF-kappaB and homeostasis of epithelial cells were implicated in the pathogenesis of NP. In this study we investigated the expression of insulin-like growth factor-1 receptor (IGF-1R) and inducible nitric-oxide synthase (iNOS) in NP compared to healthy NM in both the epithelial and stromal compartments. Using immunohistochemistry, frozen tissue sections of NP from 18 patients, and mucosal biopsy specimens of the inferior turbinate from 17 subjects were stained for IGF-1R and iNOS markers. Fluorescence microscopy and computerized image analysis revealed low numbers of IGF-1R-positive cells in all specimens. However, substantially increased numbers of IGF-1R-positive cells were found in NP compared to NM both within the epithelium (1.63 vs. 0.43) and stroma (3.27 vs. 1.03). Positivity for iNOS was detected within the epithelium of NP compared with NM. Numbers of iNOS-positive single cells were highly increased in NP vs. NM in both epithelial (3.83 vs. 1.08) and stromal (4.96 vs. 2.67) compartments. An increased iNOS expression within the epithelial layer as well as increased number of iNOS- and IGF-1R-positive cells in NP was observed. This suggests that innate immune mechanism, and to a lesser extent also growth and homeostasis of epithelial cells, may play a role in formation of NP.

• MeSH
• biopsie MeSH
• buňky stromatu imunologie   metabolismus   patologie   MeSH
• cytokiny metabolismus   MeSH
• epitelové buňky imunologie   metabolismus   patologie   MeSH
• fluorescenční mikroskopie MeSH
• homeostáza MeSH
• jednoduchá slepá metoda MeSH
• lidé MeSH
• NF-kappa B metabolismus   MeSH
• nosní polypy chemie   etiologie   imunologie   MeSH
• nosní sliznice chemie   MeSH
• přirozená imunita MeSH
• receptor IGF typ 1 analýza   MeSH
• synthasa oxidu dusnatého, typ II analýza   MeSH
• vystavení vlivu životního prostředí MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• cytokiny MeSH
• NF-kappa B MeSH
• NOS2 protein, human MeSH Prohlížeč
• receptor IGF typ 1 MeSH
• synthasa oxidu dusnatého, typ II MeSH

Cell adhesion molecules P-selectin, VCAM-1 and ICAM-1 play an important role in the pathogenesis of atherosclerosis. High levels of nitric oxide (NO) produced by inducible NO synthase (iNOS) have been associated with atherosclerotic processes. Simvastatin is an HMG-CoA reductase inhibitor responsible for many clinical benefits. The aim of this study was to detect and quantify changes in endothelial expression of P-selectin, VCAM-1, ICAM-1 and iNOS in the vessel wall after the shortterm administration of simvastatin in a rabbit model of atherosclerosis. Eighteen New Zealand White rabbits were randomly divided into three groups (n=6). In the cholesterol group, rabbits consumed an atherogenic diet (0.4% cholesterol) for eight weeks. In the simvastatin group, rabbits consumed an atherogenic diet for six weeks and then consumed an atherogenic diet supplemented with simvastatin (10 mg kg(-1)) for two weeks. Biochemical analysis showed that administration of simvastatin led to an almost two-fold lowering of the total serum cholesterol, VLDL, LDL and HDL, but not triglycerides, compared with the cholesterol-fed rabbits only. Stereological analysis of the immunohistochemical staining revealed that administration of simvastatin (10 mg kg(-1) daily) in an atherogenic diet decreased the endothelial expression of P-selectin, ICAM-1 and iNOS in both aortic arch and carotid artery compared with the cholesterol fed-rabbits only. We conclude that simvastatin has beneficial effects on endothelial function by decreasing expression of P-selectin, ICAM-1 and iNOS in endothelial cells in the very early stages of atherogenesis.

• MeSH
• aorta thoracica patologie   fyziologie   ultrastruktura   MeSH
• arteriae carotides patologie   fyziologie   ultrastruktura   MeSH
• arterioskleróza chemicky indukované   farmakoterapie   patofyziologie   MeSH
• časové faktory MeSH
• cholesterol krev   chemie   MeSH
• dieta aterogenní MeSH
• endoteliální buňky fyziologie   MeSH
• imunohistochemie metody   MeSH
• králíci MeSH
• modely nemocí na zvířatech MeSH
• molekuly buněčné adheze krev   účinky léků   genetika   MeSH
• rozvrh dávkování léků MeSH
• simvastatin aplikace a dávkování   farmakokinetika   terapeutické užití   MeSH
• svaly hladké cévní účinky léků   enzymologie   fyziologie   MeSH
• synthasa oxidu dusnatého, typ II MeSH
• synthasa oxidu dusnatého genetika   MeSH
• zvířata MeSH
• Check Tag
• králíci MeSH
• mužské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• srovnávací studie MeSH
• Názvy látek
• cholesterol MeSH
• molekuly buněčné adheze MeSH
• simvastatin MeSH
• synthasa oxidu dusnatého, typ II MeSH
• synthasa oxidu dusnatého MeSH

Valsartan has the potential to attenuate neointimal hyperplasia and to suppress the inflammatory response. This study aimed to evaluate the role of valsartan in neointimal hyperplasia and the toll-like receptor 4 (TLR4)-nitric oxide synthase (NOS) pathway in the balloon-injured rat aorta.Forty-eight Wistar rats were randomly allocated to three groups: sham control (control), balloon-injured group (surgery), and balloon-injured+valsartan-treated group (valsartan). Rats were killed at 14 and 28 days after balloon-injury, and then the aortic tissues were collected for morphometric analysis as well as for measurements of the mRNA or protein expression of angiotensin II, angiotensin II type 1 (AT1) receptor, angiotensin II type 2 (AT2) receptor, TLR4, endothelial nitric oxide synthase (eNOS), inducible NOS (iNOS), serine/arginine-rich splicing factor 1(SRSF1) and extracellular signal regulated kinase (ERK). Valsartan at a dose of 20 mg/kg/day markedly decreased neointimal hyperplasia in the aorta of balloon-injured rats, and significantly reduced the mRNA or protein expression of TLR4, AT1 receptor, SRSF1 and phosphorylated-ERK (p-ERK) as well as the aortic levels of iNOS (all p < 0.05). Moreover, valsartan increased the eNOS level and AT2 receptor mRNA and protein expression levels (all p < 0.05). Valsartan prevented neointimal hyperplasia and inhibited SRSF1 expression and the TLR4-iNOS-ERK-AT1 receptor pathway in the balloon-injured rat aorta.

• MeSH
• aorta účinky léků   enzymologie   patologie   MeSH
• blokátory receptorů AT1 pro angiotensin II farmakologie   MeSH
• extracelulárním signálem regulované MAP kinasy metabolismus   MeSH
• fosforylace MeSH
• hyperplazie MeSH
• krysa rodu Rattus MeSH
• modely nemocí na zvířatech MeSH
• nemoci aorty farmakoterapie   enzymologie   genetika   patologie   MeSH
• neointima * MeSH
• poranění cév farmakoterapie   enzymologie   genetika   patologie   MeSH
• potkani Wistar MeSH
• receptor angiotensinu typ 1 genetika   metabolismus   MeSH
• serin-arginin sestřihové faktory metabolismus   MeSH
• signální transdukce MeSH
• synthasa oxidu dusnatého, typ II metabolismus   MeSH
• toll-like receptor 4 genetika   metabolismus   MeSH
• valsartan farmakologie   MeSH
• zvířata MeSH
• Check Tag
• krysa rodu Rattus MeSH
• mužské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• Názvy látek
• blokátory receptorů AT1 pro angiotensin II MeSH
• extracelulárním signálem regulované MAP kinasy MeSH
• Nos2 protein, rat MeSH Prohlížeč
• receptor angiotensinu typ 1 MeSH
• serin-arginin sestřihové faktory MeSH
• SRSF1 protein, rat MeSH Prohlížeč
• synthasa oxidu dusnatého, typ II MeSH
• Tlr4 protein, rat MeSH Prohlížeč
• toll-like receptor 4 MeSH
• valsartan MeSH

We studied anxiety-like behavior in the elevated plus-maze (EPM) tests in male Lewis rats on days 2 and 4 of adjuvant arthritis (AA). In plasma we analyzed C-reactive protein (CRP), albumin, ACTH, corticosterone, in the hippocampus the mRNA expression of interleukin-1β (IL-1β), interleukin-6 (IL-6), corticotrophin releasing factor (CRH), NADPH oxidases NOX1 and NOX2, and inducible NO-synthase (iNOS). EPM tests showed a higher anxiety index in AA rats on days 2 and 4 and reduction of total entries. On days 2 and 4 we found reduced plasma albumin, enhanced CRP, ACTH and corticosterone, and in the hippocampus enhanced mRNA for NOX1 and IL-1β in AA rats, on day 4 we found enhanced mRNAs for iNOS and IL-6, and reduced mRNA for CRH. The mRNA for NOX2 did not change on any experimental day. These results suggest enhanced anxiety, as well as locomotor impairment during the early phase of AA that correlate with enhanced mRNA expressions of parameters of oxidative stress NOX1, iNOS, and inflammatory cytokines IL-1β and IL-6 in the hippocampus.

• MeSH
• artritida experimentální komplikace   metabolismus   psychologie   MeSH
• bludiště - učení fyziologie   MeSH
• hipokampus metabolismus   MeSH
• interleukin-1beta biosyntéza   MeSH
• interleukin-6 biosyntéza   MeSH
• krysa rodu Rattus MeSH
• messenger RNA biosyntéza   MeSH
• NADH, NADPH oxidoreduktasy biosyntéza   MeSH
• NADPH-oxidasa 1 MeSH
• potkani inbrední LEW MeSH
• synthasa oxidu dusnatého, typ II biosyntéza   MeSH
• úzkost komplikace   metabolismus   psychologie   MeSH
• zvířata MeSH
• Check Tag
• krysa rodu Rattus MeSH
• mužské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• srovnávací studie MeSH
• Názvy látek
• interleukin-1beta MeSH
• interleukin-6 MeSH
• messenger RNA MeSH
• NADH, NADPH oxidoreduktasy MeSH
• NADPH-oxidasa 1 MeSH
• Nos2 protein, rat MeSH Prohlížeč
• NOX1 protein, rat MeSH Prohlížeč
• synthasa oxidu dusnatého, typ II MeSH

Two major effector systems are frequently implicated in the immune and endothelial cell alternations associated with inflammation. They include the enhanced production of reactive oxygen species and diminished bioavailability of nitric oxide (NO). Importantly, these processes can be regulated by endogenously produced methylarginines, inhibitors for NO derived from macrophages and endothelial cells. Therefore, the aim of this study was to show the potential pharmacological intervention of methylarginines (N(G)-methyl-L-arginine, L-NMMA; N(G), N(G)'-dimethyl-L-arginine-symmetric dimethylarginine, SDMA; and N(G), N(G)-dimethyl-L-arginine-asymmetric dimethylarginine, ADMA) in activation of murine peritoneal (RAW 264.7) and alveolar (MHS) macrophages with lipopolysaccharide from Gram-negative bacteria (LPS). The data presented in this study clearly declare that L-NMMA (1-50μM) and ADMA (10-50 μM) significantly inhibited the LPS-induced NO production from macrophages in a concentration-dependent manner. It was demonstrated, for the first time, that the ADMA- and L-NMMA-induced down regulation of NO production was accompanied by reduced expression of mRNA and protein for inducible NO synthase as well as decreased activation of nuclear factor-κB. Importantly, we found a negative correlation between the ADMA-dependent reduction of NO production and ADMA-increased superoxide formation, which indicates that ADMA can negatively affect the balance in LPS-induced macrophage-derived production of reactive mediators. The only effect of SDMA was observed for LPS-triggered superoxide production, which was significantly decreased in its highest concentration (50 μM). In summary, L-NMMA and ADMA can mediate their effects on macrophage activation via regulation of intracellular signaling pathways, which can affect critical functions in activated macrophages.

• MeSH
• alveolární makrofágy účinky léků   imunologie   metabolismus   MeSH
• arginin analogy a deriváty   chemie   farmakologie   MeSH
• buněčné kultury MeSH
• buněčné linie MeSH
• exprese genu účinky léků   MeSH
• lipopolysacharidy toxicita   MeSH
• myši MeSH
• NF-kappa B antagonisté a inhibitory   biosyntéza   genetika   MeSH
• oxid dusnatý biosyntéza   MeSH
• peritoneální makrofágy účinky léků   imunologie   metabolismus   MeSH
• polymerázová řetězová reakce s reverzní transkripcí MeSH
• superoxidy metabolismus   MeSH
• synthasa oxidu dusnatého, typ II antagonisté a inhibitory   biosyntéza   genetika   MeSH
• viabilita buněk účinky léků   MeSH
• vztah mezi dávkou a účinkem léčiva MeSH
• western blotting MeSH
• zvířata MeSH
• Check Tag
• myši MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• arginin MeSH
• dimethylarginine MeSH Prohlížeč
• lipopolysaccharide, E. coli O26-B6 MeSH Prohlížeč
• lipopolysacharidy MeSH
• NF-kappa B MeSH
• Nos2 protein, mouse MeSH Prohlížeč
• oxid dusnatý MeSH
• superoxidy MeSH
• synthasa oxidu dusnatého, typ II MeSH