PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 7514190-6 1994 Combinations of cytokines, notably IL-1 beta plus IFN-gamma plus TNF-alpha, induced increased expression of inducible NO synthase mRNA after 6 h and resulted in a fivefold increase in medium nitrite accumulation after 48 h. These cytokines did not impair glucose metabolism or insulin release in response to 16.7 mM glucose, but there was an 80% decrease in islet insulin content. Glucose 255-262 nitric oxide synthase 2 Homo sapiens 108-129 34953892-9 2022 Western blotting showed a higher level of SREBP2, iNOS, and VEGF and a lower eNOS level in the higher glucose groups. Glucose 102-109 nitric oxide synthase 2 Homo sapiens 50-54 34402957-5 2021 The LPS-induced increases in inducible nitric oxide (NO) synthase (iNOS) expression and NO production were also significantly enhanced by long-term exposure of macrophages to high glucose. Glucose 180-187 nitric oxide synthase 2 Homo sapiens 67-71 31410144-11 2019 In conclusion, the current study demonstrated that lncRNA SCAL1 inhibits iNOS protein expression in lung cells under high-glucose conditions, which suggests that SCAL1 may have potential in the treatment of patients with diabetic lung disease. Glucose 122-129 nitric oxide synthase 2 Homo sapiens 73-77 34252390-5 2021 The present study examined the involvement of the NO synthase (NOS)/NO pathway in the regulation of SIRT1-AMPK signaling and glucose uptake in podocytes. Glucose 125-132 nitric oxide synthase 2 Homo sapiens 50-61 35607962-5 2022 We found that high glucose level decreases cell viability and increases COX2 and iNOS expressions in HUVECs. Glucose 19-26 nitric oxide synthase 2 Homo sapiens 81-85 35607962-6 2022 Our data also indicated that ELF3 overexpression participates in high glucose-mediated cell viability reduction and high glucose-induced COX2 and iNOS expressions. Glucose 121-128 nitric oxide synthase 2 Homo sapiens 146-150 35607962-12 2022 In conclusion, propofol downregulates high glucose-induced SP1 expression, thus attenuating high glucose-induced ELF3 expression, inhibiting high glucose-induced COX2 and iNOS expressions, and improving high glucose-mediated cell viability reduction in HUVECs. Glucose 146-153 nitric oxide synthase 2 Homo sapiens 171-175 31672462-5 2020 Accumulating evidence strongly imply that iNOS-derived NO plays a central role in the regulation of several biochemical pathways and energy metabolism including glucose and lipid metabolism during inflammatory conditions. Glucose 161-168 nitric oxide synthase 2 Homo sapiens 42-46 31672462-6 2020 This review summarizes current evidence for the regulation of glucose and lipid metabolism by iNOS during inflammation, and argues for the role of iNOS as a metabolic enzyme in immune and non-immune cells. Glucose 62-69 nitric oxide synthase 2 Homo sapiens 94-98 30696869-5 2019 Biochemical parameters were assayed and showed that the shift from normal glucose (NG; 5.5 mM) to high glucose (HG; 25 mM) promoted cell growth and induced oxidative/inflammatory stress and microglial activation, as evidenced by increased MTT reduction, elevated pro-inflammatory factor secretion (i.e., TNF-alpha and oxygen free radicals), and upregulated expression of stress/inflammatory proteins (i.e., HSP70, HO-1, iNOS, and COX-2). Glucose 103-110 nitric oxide synthase 2 Homo sapiens 420-424 31410144-0 2019 lncRNA SCAL1 inhibits inducible nitric oxide synthase in lung cells under high-glucose conditions. Glucose 79-86 nitric oxide synthase 2 Homo sapiens 22-53 31410144-7 2019 Expression levels of iNOS and NO production following treatment with high (30 mM) glucose were examined by western blot analysis and NO assay, respectively. Glucose 82-89 nitric oxide synthase 2 Homo sapiens 21-25 31410144-10 2019 Furthermore, the overexpression of SCAL1 inhibited iNOS protein expression and reduced NO production in cells treated with high glucose. Glucose 128-135 nitric oxide synthase 2 Homo sapiens 51-55 30423993-9 2018 The inducible nitric oxide synthase (iNOS) enzyme responsible for NO production was upregulated in normal and high glucose conditions and the proliferation rate of fibroblasts was not statistically different in all the treatment groups. Glucose 115-122 nitric oxide synthase 2 Homo sapiens 4-35 30423993-9 2018 The inducible nitric oxide synthase (iNOS) enzyme responsible for NO production was upregulated in normal and high glucose conditions and the proliferation rate of fibroblasts was not statistically different in all the treatment groups. Glucose 115-122 nitric oxide synthase 2 Homo sapiens 37-41 28565879-6 2017 Exposure of human umbilical vein endothelial cells (HUVEC) to a high glucose concentration decreased NO and endothelial nitric oxide synthase (eNOS) levels but increased inducible NOS (iNOS) levels. Glucose 69-76 nitric oxide synthase 2 Homo sapiens 170-183 28555668-3 2017 A glucose-sensitive signal transduction circuit involving the mTOR complex 1 (mTORC1), HIF1alpha and inducible nitric oxide synthase (iNOS) coordinates DC metabolism and function to limit DC-stimulated T-cell responses. Glucose 2-9 nitric oxide synthase 2 Homo sapiens 101-132 28555668-3 2017 A glucose-sensitive signal transduction circuit involving the mTOR complex 1 (mTORC1), HIF1alpha and inducible nitric oxide synthase (iNOS) coordinates DC metabolism and function to limit DC-stimulated T-cell responses. Glucose 2-9 nitric oxide synthase 2 Homo sapiens 134-138 28565879-6 2017 Exposure of human umbilical vein endothelial cells (HUVEC) to a high glucose concentration decreased NO and endothelial nitric oxide synthase (eNOS) levels but increased inducible NOS (iNOS) levels. Glucose 69-76 nitric oxide synthase 2 Homo sapiens 185-189 28188286-8 2017 iNOS siRNA and 1400W, a selective iNOS inhibitor, abolished the ameliorative effects of NaHS on high glucose-induced NOX4 expression, reactive oxygen species generation, and, matrix laminin expression. Glucose 101-108 nitric oxide synthase 2 Homo sapiens 0-4 28188286-8 2017 iNOS siRNA and 1400W, a selective iNOS inhibitor, abolished the ameliorative effects of NaHS on high glucose-induced NOX4 expression, reactive oxygen species generation, and, matrix laminin expression. Glucose 101-108 nitric oxide synthase 2 Homo sapiens 34-38 28188286-9 2017 Thus, H2S recruits iNOS to generate NO to inhibit high glucose-induced NOX4 expression, oxidative stress, and matrix protein accumulation in renal epithelial cells; the two gasotransmitters H2S and NO and their interaction may serve as therapeutic targets in diabetic kidney disease. Glucose 55-62 nitric oxide synthase 2 Homo sapiens 19-23 27927986-5 2017 Glucose itself dose dependently increased LPS-induced iNOS expression. Glucose 0-7 nitric oxide synthase 2 Homo sapiens 54-58 28157664-3 2017 We found that lowering the glucose concentration increased expression of genes coding for inducible nitric oxide syntheas, NOS2 and NOS2A resulting in enhanced production of nitric oxide. Glucose 27-34 nitric oxide synthase 2 Homo sapiens 123-127 28157664-3 2017 We found that lowering the glucose concentration increased expression of genes coding for inducible nitric oxide syntheas, NOS2 and NOS2A resulting in enhanced production of nitric oxide. Glucose 27-34 nitric oxide synthase 2 Homo sapiens 132-137 27927986-7 2017 The activity of LPS-induced nuclear factor-kappaB (NF-kappaB) and DNA binding of c-Rel to the iNOS promoter were inhibited under high glucose conditions in comparison with no significant changes under normal glucose conditions. Glucose 134-141 nitric oxide synthase 2 Homo sapiens 94-98 27927986-7 2017 The activity of LPS-induced nuclear factor-kappaB (NF-kappaB) and DNA binding of c-Rel to the iNOS promoter were inhibited under high glucose conditions in comparison with no significant changes under normal glucose conditions. Glucose 208-215 nitric oxide synthase 2 Homo sapiens 94-98 27927986-8 2017 In addition, we found that the LPS-induced increase in O-GlcNAcylation as well as DNA binding of c-Rel to the iNOS promoter were further increased by GlcN under normal glucose conditions. Glucose 168-175 nitric oxide synthase 2 Homo sapiens 110-114 27927986-10 2017 The NF-kappaB inhibitor, pyrrolidine dithiocarbamate, inhibited LPS-induced iNOS expression under high glucose conditions but it did not influence iNOS induction under normal glucose conditions. Glucose 103-110 nitric oxide synthase 2 Homo sapiens 76-80 27927986-12 2017 By blocking transcription with actinomycin D, we found that stability of LPS-induced iNOS mRNA was increased by GlcN under normal glucose conditions. Glucose 130-137 nitric oxide synthase 2 Homo sapiens 85-89 23909711-1 2014 Abstract Glucose has been found to impair the inhibition of platelets with aspirin and alter the basal activity of nitric oxide synthase (NOS) in platelets. Glucose 9-16 nitric oxide synthase 2 Homo sapiens 115-136 26756092-5 2016 High glucose levels induced the overexpression of inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), and NF-kappaB proteins in HUVECs, which was suppressed by treatment with 0.04 mM daidzein. Glucose 5-12 nitric oxide synthase 2 Homo sapiens 50-81 26756092-5 2016 High glucose levels induced the overexpression of inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), and NF-kappaB proteins in HUVECs, which was suppressed by treatment with 0.04 mM daidzein. Glucose 5-12 nitric oxide synthase 2 Homo sapiens 83-87 25086922-5 2014 In addition, high glucose levels induced the overexpressions of inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), and nuclear factor-kappa B (NF-kappaB) proteins in HUVECs, but BEK treatment reduced the overexpressions of these proteins. Glucose 18-25 nitric oxide synthase 2 Homo sapiens 64-95 25086922-5 2014 In addition, high glucose levels induced the overexpressions of inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), and nuclear factor-kappa B (NF-kappaB) proteins in HUVECs, but BEK treatment reduced the overexpressions of these proteins. Glucose 18-25 nitric oxide synthase 2 Homo sapiens 97-101 25894234-9 2015 eNOS and iNOS gene expression was increased in HUVEC cells after different concentrations and time periods of glucose treatment. Glucose 110-117 nitric oxide synthase 2 Homo sapiens 9-13 24896242-16 2014 ACS14, aspirin and NaHS attenuated the increase in iNOS expression caused by high glucose (25 mM). Glucose 82-89 nitric oxide synthase 2 Homo sapiens 51-55 24699383-8 2014 In vitro study showed that treatment with GSNO under high glucose condition counteracted nitrosative stress due to iNOS downregulation by S-glutathionylation, and not by prevention of decreased GSNO and reduced glutathione levels. Glucose 58-65 nitric oxide synthase 2 Homo sapiens 115-119 23801050-8 2013 Superoxide, peroxynitrite, TGF-beta, and fibronectin productions as well as the protein expressions of NOX1, NOX2, NOX4, and iNOS were increased in the diabetic milieu (high glucose 30 mmol/L plus AGE 200 mg/L). Glucose 174-181 nitric oxide synthase 2 Homo sapiens 125-129 24177007-0 2013 ER stress-mediated regulation of immune function under glucose-deprived condition in glial cells: up- and down-regulation of PGE2 + IFNgamma-induced IL-6 and iNOS expressions. Glucose 55-62 nitric oxide synthase 2 Homo sapiens 158-162 24177007-4 2013 On the other hand, to our surprise, we found that PGE2+IFNgamma-induced iNOS expression was attenuated under glucose-deprived condition. Glucose 109-116 nitric oxide synthase 2 Homo sapiens 72-76 23454417-0 2013 Protein nitration promotes inducible nitric oxide synthase transcription mediated by NF-kappaB in high glucose-stimulated human lens epithelial cells. Glucose 103-110 nitric oxide synthase 2 Homo sapiens 27-58 23812491-0 2013 Regulation of iNOS expression by NF-kappaB in human lens epithelial cells treated with high levels of glucose. Glucose 102-109 nitric oxide synthase 2 Homo sapiens 14-18 23812491-1 2013 PURPOSE: To explore the regulation of inducible nitric oxide synthase (iNOS) expression by nuclear factor kappa B (NF-kappaB) in human lens epithelial cells (LECs) treated with high levels of glucose, and to elucidate the impact of this in the pathogenesis of cataracts associated with diabetes. Glucose 192-199 nitric oxide synthase 2 Homo sapiens 38-69 23812491-1 2013 PURPOSE: To explore the regulation of inducible nitric oxide synthase (iNOS) expression by nuclear factor kappa B (NF-kappaB) in human lens epithelial cells (LECs) treated with high levels of glucose, and to elucidate the impact of this in the pathogenesis of cataracts associated with diabetes. Glucose 192-199 nitric oxide synthase 2 Homo sapiens 71-75 23812491-10 2013 iNOS mRNA and protein levels also increased significantly in a time- and concentration-dependent manner and iNOS mRNA and protein reached their peak values after 8 hours of treatment with 25 mM glucose. Glucose 194-201 nitric oxide synthase 2 Homo sapiens 0-4 23812491-10 2013 iNOS mRNA and protein levels also increased significantly in a time- and concentration-dependent manner and iNOS mRNA and protein reached their peak values after 8 hours of treatment with 25 mM glucose. Glucose 194-201 nitric oxide synthase 2 Homo sapiens 108-112 23812491-11 2013 The binding of NF-kappaB to the promoter of the iNOS gene was enhanced in the 25 mM glucose group compared with the 5.5 mM glucose group or the 25 mM glucose + 100 muL PDTC group, and this difference was statistically significant (P < 0.05). Glucose 84-91 nitric oxide synthase 2 Homo sapiens 48-52 23812491-11 2013 The binding of NF-kappaB to the promoter of the iNOS gene was enhanced in the 25 mM glucose group compared with the 5.5 mM glucose group or the 25 mM glucose + 100 muL PDTC group, and this difference was statistically significant (P < 0.05). Glucose 123-130 nitric oxide synthase 2 Homo sapiens 48-52 23812491-11 2013 The binding of NF-kappaB to the promoter of the iNOS gene was enhanced in the 25 mM glucose group compared with the 5.5 mM glucose group or the 25 mM glucose + 100 muL PDTC group, and this difference was statistically significant (P < 0.05). Glucose 123-130 nitric oxide synthase 2 Homo sapiens 48-52 23812491-13 2013 Under high glucose conditions, NF-kappaB is activated and rapidly translocates to the nucleus, leading to increased binding to the iNOS promoter and a consequent increase in iNOS expression. Glucose 11-18 nitric oxide synthase 2 Homo sapiens 131-135 23812491-13 2013 Under high glucose conditions, NF-kappaB is activated and rapidly translocates to the nucleus, leading to increased binding to the iNOS promoter and a consequent increase in iNOS expression. Glucose 11-18 nitric oxide synthase 2 Homo sapiens 174-178 23773265-0 2013 Effect of nitric oxide synthase inhibition on the exchange of glucose and fatty acids in human skeletal muscle. Glucose 62-69 nitric oxide synthase 2 Homo sapiens 10-31 23454417-5 2013 Moreover, nearly all predicted NF-kappaB binding sites in the human iNOS gene promoter were responsive to high glucose stimulation, might for a synergistic role. Glucose 111-118 nitric oxide synthase 2 Homo sapiens 68-72 23454417-6 2013 While, only the NF-kappaB binding site -5212 showed significant alterations by high glucose and peroxynitrite stimulations, indicating it a more important role in the protein nitration promoted iNOS gene transcription. Glucose 84-91 nitric oxide synthase 2 Homo sapiens 194-198 23454417-7 2013 Our results demonstrated that protein nitration can promote the NF-kappaB-activated iNOS gene transcription in human lens epithelial cells by high glucose stimulation. Glucose 147-154 nitric oxide synthase 2 Homo sapiens 84-88 22687049-6 2012 Culture of diabetic islets at 5.5 mmol/l glucose with dibutyryl-cAMP (Bt(2) -cAMP) for 24 h was accompanied by marked suppression of iNOS mRNA, reduced nitrite production and increased insulin secretion. Glucose 41-48 nitric oxide synthase 2 Homo sapiens 133-137 22687049-11 2012 Defective glucose-stimulated insulin release upon induction of iNOS was restored by iNOS inhibitor aminoguanidine. Glucose 10-17 nitric oxide synthase 2 Homo sapiens 63-67 22687049-11 2012 Defective glucose-stimulated insulin release upon induction of iNOS was restored by iNOS inhibitor aminoguanidine. Glucose 10-17 nitric oxide synthase 2 Homo sapiens 84-88 22687049-12 2012 CONCLUSION: Our results suggest that in islets from type 2 diabetes, stimulatory effects in certain cAMP-compartments induced by PDE inhibitors might play a central role in the suppression of iNOS, resulting in increased beta-cell viability and improved secretory response to glucose. Glucose 276-283 nitric oxide synthase 2 Homo sapiens 192-196 21236251-6 2011 We prepared AGEs, established the high glucose-AGEs injured microEC models by MTT assay, which was further supported by significantly decreased nitric oxide (NO) release, NO synthase (NOS) and thrombomodulin production with ELISA, western blot and RT-PCR analysis. Glucose 39-46 nitric oxide synthase 2 Homo sapiens 171-182 21637955-9 2012 Taken together, these data demonstrate the role of AR in regulating iNOS expression induced by TNF-alpha in cultured HMC, indicating the novel function of AR in glomerulonephritis besides glucose metabolism. Glucose 188-195 nitric oxide synthase 2 Homo sapiens 68-72 21952043-2 2012 Exposure to high glucose increased nitrated proteins (1.56 fold p<0.05), inducible nitric oxide synthase (iNOS) and neuronal NOS (nNOS) mRNA expression (1.55 fold and 2.2 fold respectively, p<0.05 both), phospho-p38 MAPK (1.32 fold, p<0.05) abundance and decreased Schwann cell growth (11+-2%, p<0.05). Glucose 17-24 nitric oxide synthase 2 Homo sapiens 76-107 21952043-2 2012 Exposure to high glucose increased nitrated proteins (1.56 fold p<0.05), inducible nitric oxide synthase (iNOS) and neuronal NOS (nNOS) mRNA expression (1.55 fold and 2.2 fold respectively, p<0.05 both), phospho-p38 MAPK (1.32 fold, p<0.05) abundance and decreased Schwann cell growth (11+-2%, p<0.05). Glucose 17-24 nitric oxide synthase 2 Homo sapiens 109-113 21952043-3 2012 Taurine supplementation prevented high-glucose induced iNOS and nNOS mRNA upregulation, reduced nitrated proteins and phospho-p38 MAPK (56+-11% and 45+-18% (p<0.05 both) respectively) and restored Schwann cell growth to control levels. Glucose 39-46 nitric oxide synthase 2 Homo sapiens 55-59 22425406-5 2012 RESULTS: SOD1 treatment diminished high glucose-induced oxidative stress, as evidenced by 4-hydroxynonenal and malondialdehyde reductions, and it blocked high glucose-increased iNOS expression, iNOS-luciferase activities, and nitrosylated protein. Glucose 159-166 nitric oxide synthase 2 Homo sapiens 177-181 22363694-0 2012 High glucose decreases expression and activity of p-glycoprotein in cultured human retinal pigment epithelium possibly through iNOS induction. Glucose 5-12 nitric oxide synthase 2 Homo sapiens 127-131 21311355-1 2011 PURPOSE: We have previously shown that local infusion of a nitric oxide synthase (NOS) inhibitor attenuates increases in leg glucose uptake during exercise in humans. Glucose 125-132 nitric oxide synthase 2 Homo sapiens 59-80 21435358-5 2011 Furthermore, SP600125 (a specific inhibitor of JNK) and 1400W (a specific inhibitor of iNOS) significantly attenuated cell apoptosis induced by high glucose. Glucose 149-156 nitric oxide synthase 2 Homo sapiens 87-91 18854222-6 2009 Treatment of RPE cells with high glucose-induced a significant increased of iNOS, accompanied by an increase in cell damage, NO and nitrotyrosine levels. Glucose 33-40 nitric oxide synthase 2 Homo sapiens 76-80 18854222-7 2009 High glucose caused activation of p38MAPK and ERK, inhibition for p38MAPK and ERK abrogated the high glucose-induced increase in iNOS, cell injury and levels of NO and nitrotyrosine. Glucose 5-12 nitric oxide synthase 2 Homo sapiens 129-133 18854222-7 2009 High glucose caused activation of p38MAPK and ERK, inhibition for p38MAPK and ERK abrogated the high glucose-induced increase in iNOS, cell injury and levels of NO and nitrotyrosine. Glucose 101-108 nitric oxide synthase 2 Homo sapiens 129-133 18854222-8 2009 High glucose causes increased cell damage and NO generation in RPE cells by a process of iNOS expression that requires the activation of p38MAPK and ERK. Glucose 5-12 nitric oxide synthase 2 Homo sapiens 89-93 16641887-1 2006 Pyruvic acid, an intermediate metabolite of glucose, an effective scavenger of reactive oxygen species (ROS), inhibits tumor necrosis factor-alpha production and NF-kappaB signaling pathways, reduces circulating levels of HMGB1 (high mobility group B1), decreases COX-2 (cyclo-oxygenase-2), iNOS (inducible nitric oxide synthase), and IL-6 (interleukin-6) mRNA expression in liver, ileal mucosa, and colonic mucosa in animal models with endotoxemia. Glucose 44-51 nitric oxide synthase 2 Homo sapiens 291-295 17881613-0 2007 Local nitric oxide synthase inhibition reduces skeletal muscle glucose uptake but not capillary blood flow during in situ muscle contraction in rats. Glucose 63-70 nitric oxide synthase 2 Homo sapiens 6-27 17881613-1 2007 OBJECTIVE: We have previously shown in humans that local infusion of a nitric oxide synthase (NOS) inhibitor into the femoral artery attenuates the increase in leg glucose uptake during exercise without influencing total leg blood flow. Glucose 164-171 nitric oxide synthase 2 Homo sapiens 71-92 17067575-8 2007 Isoproterenol treatment for 6 h to human retinal endothelial cells grown in high glucose medium reduced iNOS protein expression, but had no effect on PGE2 levels or PGE2 receptor protein expression. Glucose 81-88 nitric oxide synthase 2 Homo sapiens 104-108 17721990-6 2008 Co-treatment of HUVECs with 5 microM MG and 20 mM glucose significantly increased cytoplasmic free calcium levels, activation of nitric oxide synthase (NOS), caspase-3 and -9, cytochrome c release, and apoptotic cell death. Glucose 50-57 nitric oxide synthase 2 Homo sapiens 129-150 18300858-4 2008 However, the high concentration of D-glucose did increase iNOS expression in response to low concentrations of IL-1beta (2.5 and 5 ng/ml), as well as the IL-1beta-induced activation of both ERK 1/2 and NF-kappaB. Glucose 35-44 nitric oxide synthase 2 Homo sapiens 58-62 18300858-5 2008 D-glucose also enhanced, concentration-dependently, the expression and activity of iNOS induced by co-incubation with IL-1beta (10 ng/ml). Glucose 0-9 nitric oxide synthase 2 Homo sapiens 83-87 17574318-5 2007 High glucose levels induced the overexpressions of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) proteins, but HMPPP or LMPPP treatment reduced the overexpressions of these proteins. Glucose 5-12 nitric oxide synthase 2 Homo sapiens 51-82 17574318-5 2007 High glucose levels induced the overexpressions of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) proteins, but HMPPP or LMPPP treatment reduced the overexpressions of these proteins. Glucose 5-12 nitric oxide synthase 2 Homo sapiens 84-88 17240121-4 2007 Increased superoxide production, induction of inducible nitric oxide synthase (iNOS), and decreased caveolin-1 were observed in a concentration-dependent manner in THP-1 derived macrophages with high glucose concentrations. Glucose 200-207 nitric oxide synthase 2 Homo sapiens 46-77 17240121-4 2007 Increased superoxide production, induction of inducible nitric oxide synthase (iNOS), and decreased caveolin-1 were observed in a concentration-dependent manner in THP-1 derived macrophages with high glucose concentrations. Glucose 200-207 nitric oxide synthase 2 Homo sapiens 79-83 16641887-1 2006 Pyruvic acid, an intermediate metabolite of glucose, an effective scavenger of reactive oxygen species (ROS), inhibits tumor necrosis factor-alpha production and NF-kappaB signaling pathways, reduces circulating levels of HMGB1 (high mobility group B1), decreases COX-2 (cyclo-oxygenase-2), iNOS (inducible nitric oxide synthase), and IL-6 (interleukin-6) mRNA expression in liver, ileal mucosa, and colonic mucosa in animal models with endotoxemia. Glucose 44-51 nitric oxide synthase 2 Homo sapiens 297-328 15591036-2 2004 The aim of the study was to assess the effects of inflammatory cytokines and oxidative stress associated with increased glucose concentrations on inducible nitric oxide synthase (iNOS) promoter activity in intestinal epithelial cells. Glucose 120-127 nitric oxide synthase 2 Homo sapiens 179-183 16472125-0 2006 High glucose-mediated imbalance of nitric oxide synthase and dimethylarginine dimethylaminohydrolase expression in endothelial cells. Glucose 5-12 nitric oxide synthase 2 Homo sapiens 35-56 16472125-6 2006 Data obtained in the present study show that the exposure for 5 days to high glucose increases oxidative stress, reduces DDAH-2 and eNOS expression and increases iNOS expression. Glucose 77-84 nitric oxide synthase 2 Homo sapiens 162-166 16472125-7 2006 These results indicate that DDAH-2 and iNOS/eNOS dysregulation may play a key role in high glucose-mediated oxidative stress, suggesting that selective modulation of DDAH isoforms may result in selective inhibition/activation of NOS isoforms, thereby providing a novel strategy of approach in vascular complications of several pathologies. Glucose 91-98 nitric oxide synthase 2 Homo sapiens 39-43 15591036-5 2004 Upregulation of basal iNOS promoter activity was observed when cells were incubated in high glucose alone. Glucose 92-99 nitric oxide synthase 2 Homo sapiens 22-26 15591036-9 2004 In conclusion, iNOS promoter activity induced by high concentrations of glucose is mediated in part through intracellular GSH and NFkappaB. Glucose 72-79 nitric oxide synthase 2 Homo sapiens 15-19 12824867-1 2003 OBJECTIVE: It is well known that nitric oxide synthase (NOS) is expressed and that it modulates glucose transport in skeletal muscles. Glucose 96-103 nitric oxide synthase 2 Homo sapiens 33-54 15099358-0 2004 Inhibition of nuclear factor kappa B activation and inducible nitric oxide synthase transcription by prolonged exposure to high glucose in the human keratinocyte cell line HaCaT. Glucose 128-135 nitric oxide synthase 2 Homo sapiens 52-83 15099358-2 2004 We speculated that diabetic skin complications such as delayed wound healing and skin infection were due to iNOS activity altered by high glucose in skin keratinocytes. Glucose 138-145 nitric oxide synthase 2 Homo sapiens 108-112 15099358-3 2004 OBJECTIVES: The purpose of this study was to see how high levels of glucose affect iNOS activity in the human keratinocyte cell line (HaCaT). Glucose 68-75 nitric oxide synthase 2 Homo sapiens 83-87 15099358-6 2004 RESULTS: Short-term exposure (1 day) to a high level of glucose increased BH(4) and iNOS activity at the post-translational level. Glucose 56-63 nitric oxide synthase 2 Homo sapiens 84-88 15099358-7 2004 However, long-term exposure (10 days) to high glucose downregulates NF-kappaB binding activity and inhibits iNOS transcription and its activity. Glucose 46-53 nitric oxide synthase 2 Homo sapiens 108-112 15099358-8 2004 CONCLUSIONS: Pretreatment with high glucose for 10 days down-regulated NF-kappaB activity and inhibited iNOS transcription and NO production, implying the involvement of a deficiency in NO synthesis in both skin infection and impaired wound healing in diabetic patients. Glucose 36-43 nitric oxide synthase 2 Homo sapiens 104-108 15591036-0 2004 High glucose decreases intracellular glutathione concentrations and upregulates inducible nitric oxide synthase gene expression in intestinal epithelial cells. Glucose 5-12 nitric oxide synthase 2 Homo sapiens 80-111 15591036-2 2004 The aim of the study was to assess the effects of inflammatory cytokines and oxidative stress associated with increased glucose concentrations on inducible nitric oxide synthase (iNOS) promoter activity in intestinal epithelial cells. Glucose 120-127 nitric oxide synthase 2 Homo sapiens 146-177 15351621-10 2004 RESULTS: The least expression of endothelial NOS (eNOS) and inducible NOS (iNOS) in HCSMCs was observed in cells exposed to 27 mM glucose alone. Glucose 130-137 nitric oxide synthase 2 Homo sapiens 60-73 15351621-10 2004 RESULTS: The least expression of endothelial NOS (eNOS) and inducible NOS (iNOS) in HCSMCs was observed in cells exposed to 27 mM glucose alone. Glucose 130-137 nitric oxide synthase 2 Homo sapiens 75-79 9867221-1 1998 Recent studies have shown that cytokines and endotoxins impair insulin-stimulated glucose transport by activating the expression of inducible nitric oxide synthase (iNOS) and nitric oxide (NO) production in skeletal muscle cells. Glucose 82-89 nitric oxide synthase 2 Homo sapiens 132-163 12055099-7 2002 The data strongly suggest, but do not definitely prove, that glucose indeed has the ability to stimulate both cNOS and iNOS in the islets and that NO might serve as a negative feedback inhibitor of glucose-stimulated insulin release. Glucose 61-68 nitric oxide synthase 2 Homo sapiens 119-123 10511689-2 1999 When combined with the newly recognized roles of iNOS in renal and pulmonary function and glucose metabolism, synergy between inflammatory cytokines and hypoxia in iNOS induction provides a framework to help explain, at a molecular level, the differences in the pathology seen in falciparum and vivax malaria. Glucose 90-97 nitric oxide synthase 2 Homo sapiens 164-168 10401981-5 1999 A 2-day immunostimulation, however, markedly enhanced the apoptotic death of CGC glucose-deprived for 1 h. The increased apoptotic death of glucose-deprived CGC after immunostimulation was mimicked by the nitric oxide (NO) releasing reagent 3-morpholinosydnonimine (200 microM, 30 min) and was partially prevented by the NO synthase (NOS) inhibitor N(G)-nitroarginine. Glucose 81-88 nitric oxide synthase 2 Homo sapiens 321-332 10401981-5 1999 A 2-day immunostimulation, however, markedly enhanced the apoptotic death of CGC glucose-deprived for 1 h. The increased apoptotic death of glucose-deprived CGC after immunostimulation was mimicked by the nitric oxide (NO) releasing reagent 3-morpholinosydnonimine (200 microM, 30 min) and was partially prevented by the NO synthase (NOS) inhibitor N(G)-nitroarginine. Glucose 140-147 nitric oxide synthase 2 Homo sapiens 321-332 9867221-1 1998 Recent studies have shown that cytokines and endotoxins impair insulin-stimulated glucose transport by activating the expression of inducible nitric oxide synthase (iNOS) and nitric oxide (NO) production in skeletal muscle cells. Glucose 82-89 nitric oxide synthase 2 Homo sapiens 165-169 9453318-8 1998 IL-1beta-stimulated [3H] citrulline-forming activity of the nitric oxide synthase (NOS) was also significantly lower in high-glucose-exposed cells, and this was reflected in diminished cellular levels of NOS protein. Glucose 125-132 nitric oxide synthase 2 Homo sapiens 60-81 9691088-3 1998 Treatment of human islets with a combination of tumor necrosis factor (TNF) + lipopolysaccharide (LPS) + interferon-gamma (IFN-gamma) stimulates inducible nitric oxide synthase (iNOS) expression, nitric oxide production, and inhibits glucose-stimulated insulin secretion. Glucose 234-241 nitric oxide synthase 2 Homo sapiens 178-182 9653515-0 1998 The nitric oxide synthase inhibitor NG-nitro-L-arginine methyl ester potentiates insulin secretion stimulated by glucose and L-arginine independently of its action on ATP-sensitive K+ channels. Glucose 113-120 nitric oxide synthase 2 Homo sapiens 4-25 9453318-0 1998 Calcium and protein kinase C mediate high-glucose-induced inhibition of inducible nitric oxide synthase in vascular smooth muscle cells. Glucose 42-49 nitric oxide synthase 2 Homo sapiens 82-103 9604873-0 1998 Constitutive nitric oxide synthase expression in retinal vascular endothelial cells is suppressed by high glucose and advanced glycation end products. Glucose 106-113 nitric oxide synthase 2 Homo sapiens 13-34 9230132-12 1997 These results demonstrate that cytokines and LPS affect glucose transport and insulin action by inducing iNOS expression and NO production in skeletal muscle cells. Glucose 56-63 nitric oxide synthase 2 Homo sapiens 105-109