PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 28979673-10 2017 Inhibition of COX-2 by using a specific COX-2 inhibitor NS-398 markedly blocked cell apoptosis, inflammation, and PGE2 secretion. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 56-62 cytochrome c oxidase II, mitochondrial Mus musculus 14-19 29636886-6 2018 Then a specific COX-2 inhibitor (NS-398) was administered to BV2 before LPS treatment. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 33-39 cytochrome c oxidase II, mitochondrial Mus musculus 16-21 32961332-8 2020 Finally, treatment with a COX-2 specific inhibitor, NS-398, attenuated I/R-induced injury, total peroxidase level, and PGE2 production in males, but not in similarly treated female mice. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 52-58 cytochrome c oxidase II, mitochondrial Mus musculus 26-31 30618773-4 2018 And NS398, a COX-2 inhibitor, inhibited LPS-induced NIH3T3 cells migration. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 4-9 cytochrome c oxidase II, mitochondrial Mus musculus 13-18 28979673-10 2017 Inhibition of COX-2 by using a specific COX-2 inhibitor NS-398 markedly blocked cell apoptosis, inflammation, and PGE2 secretion. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 56-62 cytochrome c oxidase II, mitochondrial Mus musculus 40-45 28469778-6 2017 Elevation of PGE2 induced by sevofluraneand LPS in peritoneal macrophages was inhibited by NS-398, an inhibitor of the PGE2 regulator COX-2, indicating that NS-398 blocked COX-2 mediated PGE2 synthesis. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 91-97 cytochrome c oxidase II, mitochondrial Mus musculus 134-139 28678919-5 2017 Cox-2, PI3K, AKT and mTOR expressions were detected by western blotting after bleomycin was administered together with NS-398 (an inhibitor of Cox-2). N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 119-125 cytochrome c oxidase II, mitochondrial Mus musculus 143-148 28469778-6 2017 Elevation of PGE2 induced by sevofluraneand LPS in peritoneal macrophages was inhibited by NS-398, an inhibitor of the PGE2 regulator COX-2, indicating that NS-398 blocked COX-2 mediated PGE2 synthesis. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 91-97 cytochrome c oxidase II, mitochondrial Mus musculus 172-177 28469778-6 2017 Elevation of PGE2 induced by sevofluraneand LPS in peritoneal macrophages was inhibited by NS-398, an inhibitor of the PGE2 regulator COX-2, indicating that NS-398 blocked COX-2 mediated PGE2 synthesis. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 157-163 cytochrome c oxidase II, mitochondrial Mus musculus 134-139 28469778-6 2017 Elevation of PGE2 induced by sevofluraneand LPS in peritoneal macrophages was inhibited by NS-398, an inhibitor of the PGE2 regulator COX-2, indicating that NS-398 blocked COX-2 mediated PGE2 synthesis. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 157-163 cytochrome c oxidase II, mitochondrial Mus musculus 172-177 26311457-7 2015 In order to determine whether the inhibition was related to PGE2, selective cyclooxygenase 2(COX-2) inhibitor NS398 was used to reverse this phenomenon and protein kinase A (PKA) inhibitor H89 demonstrated the mechanism through blocking cAMP/PKA signaling pathway. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 110-115 cytochrome c oxidase II, mitochondrial Mus musculus 93-98 28161224-7 2017 Treatment of tumor cells with COX-2 inhibitor NS-398 averted TCM induced phenotypic impairment of DC in vitro. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 46-52 cytochrome c oxidase II, mitochondrial Mus musculus 30-35 26683659-10 2016 Neuroprotection was achieved by PDTC and NS-398, inhibitors of NF-kappaB and COX-2, respectively. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 41-47 cytochrome c oxidase II, mitochondrial Mus musculus 77-82 26676587-6 2016 IL-6 from the myofibroblasts contributed to the amplification of the AAM phenotype; the selective COX-2 inhibitor, NS-398, significantly reduced the ability of myofibroblasts to promote an AAM phenotype. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 115-121 cytochrome c oxidase II, mitochondrial Mus musculus 98-103 26159723-11 2015 In vitro, inhibition of FoxM1 and Cox-2 with pharmacological inhibitors; Thiostrepton and NS398 resulted in efficient down-regulation of FoxM1 and Cox-2 expression along with in-activation of AKT and inhibition of colony formation, invasion and migratory capability of CRC cells. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 90-95 cytochrome c oxidase II, mitochondrial Mus musculus 34-39 26159723-11 2015 In vitro, inhibition of FoxM1 and Cox-2 with pharmacological inhibitors; Thiostrepton and NS398 resulted in efficient down-regulation of FoxM1 and Cox-2 expression along with in-activation of AKT and inhibition of colony formation, invasion and migratory capability of CRC cells. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 90-95 cytochrome c oxidase II, mitochondrial Mus musculus 147-152 25155888-11 2015 Additionally, CoCl2-induced decrease of cell viability was attenuated not only by dieckol and NAC but also by NS-398 (a selective COX-2 inhibitor). N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 110-116 cytochrome c oxidase II, mitochondrial Mus musculus 130-135 25817056-12 2015 Selective COX-2 inhibition by NS398 (10 muM) but not COX-1 inhibition by SC560 (300 muM) reduced increased afferent discharge in endotoxin pretreated animals to 5-HT, BK and mechanical ramp distension from 10 to 40 cmH2O (all p < 0.05). N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 30-35 cytochrome c oxidase II, mitochondrial Mus musculus 10-15 27064683-9 2016 Interestingly, aspirin, a non-specific cyclooxygenase (COX) inhibitor, partially blocked PAF-induced sudden death, whereas NS-398, a specific COX-2 inhibitor, completely protected mice from the lethal effects of PAF. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 123-129 cytochrome c oxidase II, mitochondrial Mus musculus 142-147 26311457-19 2015 (3) Using COX-2 inhibitor NS398 in the tumor-bearing + LPS mice, the protein and mRNA level of CCL5, PGE2 and cAMP were (7 691 +- 269) pg/ml and 159.0 +- 8.9, (2 820 +- 152) pg/ml and 4.9 +- 0.3, (465 +- 8) pg/ml and 4.3 +- 0.4, respectively, and there were significant difference (all P < 0.05), compared to before treatment. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 26-31 cytochrome c oxidase II, mitochondrial Mus musculus 10-15 25680189-5 2015 Macrophages differentiated in the presence of SC-560 (COX-1 inhibitor), NS-398 (COX-2 inhibitor) or indomethacin (COX-1/2 inhibitor) for 7 days produced more TNFalpha or IL-12p70 with enhanced p65/IkappaB phosphoylation. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 72-78 cytochrome c oxidase II, mitochondrial Mus musculus 80-85 25122761-9 2014 The effect of GX sPLA2 on GSIS was abolished when cells were treated with NS398 (a COX-2 inhibitor) or L-798,106 (a PGE2-EP3 receptor antagonist). N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 74-79 cytochrome c oxidase II, mitochondrial Mus musculus 83-88 25451690-10 2014 Selective inhibition of COX-2, using NS-398, decreased the contractile response in response to serotonin (5-HT) only in vessels from control mice. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 37-43 cytochrome c oxidase II, mitochondrial Mus musculus 24-29 23415923-6 2013 The beneficial effects of early DEX administration on survival were completely abrogated by coadministration of a selective cyclooxygenase (COX)-2 inhibitor (NS-398; 5mg/kg per day, p.o.). N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 158-164 cytochrome c oxidase II, mitochondrial Mus musculus 124-146 24924747-5 2014 Cotreatment with NS-398, a specific inhibitor of COX-2, also induced the intestinal lesion. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 17-23 cytochrome c oxidase II, mitochondrial Mus musculus 49-54 24098782-11 2013 However, daily administration of COX-2 inhibitor NS-398 significantly improved muscle contractility in both W/W(v) sham and obstruction mice. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 49-55 cytochrome c oxidase II, mitochondrial Mus musculus 33-38 23922381-5 2013 Coadministration of the COX-2-selective inhibitor NS398 or the selective PGE2R EP2 inhibitor AH6809 inhibited the increase in HGF production. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 50-55 cytochrome c oxidase II, mitochondrial Mus musculus 24-29 22363560-4 2012 The formation of PMF(2alpha) was reduced by indomethacin (a non-selective COX inhibitor), NS-398 (a selective COX-2 inhibitor) and SC-560 (a selective COX-1 inhibitor). N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 90-96 cytochrome c oxidase II, mitochondrial Mus musculus 110-115 20633531-6 2010 In macrophage:natural killer (NK) cell co-culture, propofol dramatically increased interferon-gamma (IFN-gamma) production, and the actions of propofol were mimicked by a selective COX-2 inhibitor, NS-398, as well as the selective EP4 receptor antagonist L-161,982, suggesting a role of PGE2 suppression in the upregulation of IFN-gamma production. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 198-204 cytochrome c oxidase II, mitochondrial Mus musculus 181-186 21843643-2 2011 N-(2-cyclohexyloxy-4-nitrophenyl) methanesulfonamide (NS-398) was the first in a series of isoform-selective drugs designed to preferentially inhibit COX-2, with the aim of ameliorating many of the toxic gastrointestinal side effects caused by conventional NSAID inhibition. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 0-52 cytochrome c oxidase II, mitochondrial Mus musculus 150-155 21843643-2 2011 N-(2-cyclohexyloxy-4-nitrophenyl) methanesulfonamide (NS-398) was the first in a series of isoform-selective drugs designed to preferentially inhibit COX-2, with the aim of ameliorating many of the toxic gastrointestinal side effects caused by conventional NSAID inhibition. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 54-60 cytochrome c oxidase II, mitochondrial Mus musculus 150-155 21843643-3 2011 We determined the X-ray crystal structure of murine COX-2 in complex with NS-398 utilizing synchrotron radiation to 3.0A resolution. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 74-80 cytochrome c oxidase II, mitochondrial Mus musculus 52-57 21843643-4 2011 NS-398 binds in the cyclooxygenase channel in a conformation that is different than that observed for other COX-2-selective inhibitors, such as celecoxib, with no discernible penetration into the side pocket formed in COX-2 by the isoform-specific substitutions of I434V, H513R, and I523V. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 0-6 cytochrome c oxidase II, mitochondrial Mus musculus 108-113 21843643-6 2011 Our structure validates inhibitor studies that identified Arg-120 as a molecular determinant for time-dependent inhibition of COX-2 by NS-398. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 135-141 cytochrome c oxidase II, mitochondrial Mus musculus 126-131 20697426-3 2011 We showed for the first time that activation of mBM-DC with agonist anti-CD40 monoclonal antibody (anti-CD40 mAb) dose dependently induces the synthesis of significant amounts of PGE2 via inducible expression of COX-2 enzyme, as NS-398, a COX-2-selective inhibitor reduces this upregulation. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 229-235 cytochrome c oxidase II, mitochondrial Mus musculus 212-217 21725746-7 2011 Following experimental SAH animals were treated with the specific COX-2 inhibitor, NS398, in dosages of either 10 or 30 mg/kg. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 83-88 cytochrome c oxidase II, mitochondrial Mus musculus 66-71 22110764-7 2011 The selective COX-2 inhibitor (NS398) reduced the contractile effect of serotonin in aortas from mice treated with vehicle or HS microparticles; however, this was not observed within mice treated with MetS microparticles, probably due to the ability of MetS microparticles to enhance prostacyclin. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 31-36 cytochrome c oxidase II, mitochondrial Mus musculus 14-19 21291942-2 2011 The present study was focused on the possible neuroprotective effect of selective cyclooxygenase (COX)-2-inhibitors: valdecoxib and NS-398 in 1-methyl-4-phenyl-1,2,3,6-tertahydropyridine (MPTP)-induced neurotoxicity in mice. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 132-138 cytochrome c oxidase II, mitochondrial Mus musculus 82-104 21376018-10 2011 The number of dopaminergic neurons in the SNpc was significantly reduced by MPTP treatment, while the MPTP-induced neuronal loss was minimal upon treatment with propofol or the selective COX-2 inhibitor, NS-398. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 204-210 cytochrome c oxidase II, mitochondrial Mus musculus 187-192 21679035-3 2011 The aim of this study was to elucidate the effects of NS-398 in the 1,2-dimethylhydrazine (DMH) mouse model with respect to alteration in the expression of COX-2 and E-cadherin-catenin complex. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 54-60 cytochrome c oxidase II, mitochondrial Mus musculus 156-161 21679035-5 2011 NS-398 showed reduced COX-2 immunoreactivity in adenomas with a decrease in vascular density in non-dysplastic mucosa. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 0-6 cytochrome c oxidase II, mitochondrial Mus musculus 22-27 21679035-10 2011 Our results suggest a protective role of NS-398 on tumour development associated with reduced COX-2 expression, reduced vascular density and perturbation of beta-catenin signalling pathway. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 41-47 cytochrome c oxidase II, mitochondrial Mus musculus 94-99 19799610-5 2009 Lewis lung carcinoma (LLC) cells were intravenously injected into WT mice and mice treated with the COX-2 inhibitor NS-398. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 116-122 cytochrome c oxidase II, mitochondrial Mus musculus 100-105 19998398-5 2010 Wogonin and NS-398, a COX-2 inhibitor, suppressed LPS-stimulated PGE(2) production in osteoblasts. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 12-18 cytochrome c oxidase II, mitochondrial Mus musculus 22-27 19344793-8 2009 A selective COX-2 inhibitor, NS-398, decreased osteoblast differentiation in WT but not KO cells. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 29-35 cytochrome c oxidase II, mitochondrial Mus musculus 12-17 19788894-8 2009 The non-steroidal anti-inflammatory drug, sulindac and a specific COX-2 inhibitor, NS398, were shown to act similarly in LPS-activated RAW 264.7 cells. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 83-88 cytochrome c oxidase II, mitochondrial Mus musculus 66-71 19564573-6 2009 Wild-type mice treated with NS-398 (a Cox-2 inhibitor) not only decreased PGE2 production but also attenuated tissue damage. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 28-34 cytochrome c oxidase II, mitochondrial Mus musculus 38-43 19749081-10 2009 A nonselective COX inhibitor, indomethacin, and a selective COX-2 inhibitor, N-[2-(cyclohexyloxy)-4-nitrophenyl]-methanesulfonamide (NS-398) inhibited the positive response. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 77-131 cytochrome c oxidase II, mitochondrial Mus musculus 60-65 19162088-4 2009 However, we observed impaired spatial retention in female mice treated with NS-398, suggesting a sex-dependent role of COX-2 in spatial memory of mice. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 76-82 cytochrome c oxidase II, mitochondrial Mus musculus 119-124 18845644-9 2009 Indeed, pretreatment of MVBs isolated from 1-wk STZ-treated mice with NS-398 [selective cyclooxygenase (COX)-2 inhibitor] unmasked endothelial dysfunction not evident in CTRL mice pretreated without or with NS-398. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 70-76 cytochrome c oxidase II, mitochondrial Mus musculus 88-110 19187602-8 2008 The bFGF-induced COX-2 upregulation led to enhanced PGE2 production by bEnd.3 cells, and this effect was abolished by the selective COX-2 inhibitor NS-398. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 148-154 cytochrome c oxidase II, mitochondrial Mus musculus 17-22 19609076-12 2009 The effects of ibuprofen are similar if not more beneficial than COX-2 inhibition by NS-398. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 85-91 cytochrome c oxidase II, mitochondrial Mus musculus 65-70 19187602-8 2008 The bFGF-induced COX-2 upregulation led to enhanced PGE2 production by bEnd.3 cells, and this effect was abolished by the selective COX-2 inhibitor NS-398. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 148-154 cytochrome c oxidase II, mitochondrial Mus musculus 132-137 18344612-4 2008 In addition, EPA, but not DHA, could be a substrate of cyclooxygenase (COX)-2, and we found that the stretching significantly augmented the expression of COX-2 and that a selective COX-2 inhibitor (NS-398) inhibited the combined effect of the stretching and EPA. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 198-204 cytochrome c oxidase II, mitochondrial Mus musculus 55-77 18982014-9 2008 Both ASA (5 mM) and NS-398 (COX-2 selective inhibitor <or=1 microM), but not SC-560 (COX-1 selective inhibitor <or=1 microM), attenuated IL-6 release from murine WAT in vitro and abolished its depot differences. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 20-26 cytochrome c oxidase II, mitochondrial Mus musculus 28-33 18616986-7 2008 The systemic injection of indomethacin, a non-selective cyclooxygenase (COX) inhibitor, and NS398, a selective COX-2 inhibitor, but not SC560, a selective COX-1 inhibitor, did not only ameliorate LPS-induced suppression of the newborn cell survival, they fully protected against the LPS effect. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 92-97 cytochrome c oxidase II, mitochondrial Mus musculus 111-116 18501188-8 2008 Effects in KO cells were mimicked in WT MSC cultures treated with NS-398, an inhibitor of COX-2 activity. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 66-72 cytochrome c oxidase II, mitochondrial Mus musculus 90-95 18344612-4 2008 In addition, EPA, but not DHA, could be a substrate of cyclooxygenase (COX)-2, and we found that the stretching significantly augmented the expression of COX-2 and that a selective COX-2 inhibitor (NS-398) inhibited the combined effect of the stretching and EPA. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 198-204 cytochrome c oxidase II, mitochondrial Mus musculus 154-159 18344612-4 2008 In addition, EPA, but not DHA, could be a substrate of cyclooxygenase (COX)-2, and we found that the stretching significantly augmented the expression of COX-2 and that a selective COX-2 inhibitor (NS-398) inhibited the combined effect of the stretching and EPA. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 198-204 cytochrome c oxidase II, mitochondrial Mus musculus 181-186 17921329-8 2007 NS-398 (specific COX-2 blocker) produced negligible inhibition of Cl-IBMECA-induced contraction in both WT +E and A(3)KO +E aorta. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 0-6 cytochrome c oxidase II, mitochondrial Mus musculus 17-22 17965942-9 2008 In vitro assays showed that COX2 significantly increased the rate of osteoclast formation, and this effect was reversible by the specific COX2 inhibitor NS-398. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 153-159 cytochrome c oxidase II, mitochondrial Mus musculus 28-32 17965942-9 2008 In vitro assays showed that COX2 significantly increased the rate of osteoclast formation, and this effect was reversible by the specific COX2 inhibitor NS-398. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 153-159 cytochrome c oxidase II, mitochondrial Mus musculus 138-142 17645771-6 2007 Gene expression profiling revealed that the expression of cyclooxygenase (COX)-2 was up-regulated in both subcutis colon 26 and spheroid cultures, and that COX-2 inhibitor NS-398 suppressed PTHrP production in spheroid cultures. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 172-178 cytochrome c oxidase II, mitochondrial Mus musculus 156-161 17541981-8 2007 Moreover, PA notably increased cyclooxygenase (COX)-2 protein expression, and PA-induced expression of both Bcl-2 and Bcl-xL was inhibited by NS-398, a specific inhibitor of COX-2. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 142-148 cytochrome c oxidase II, mitochondrial Mus musculus 31-53 17541981-8 2007 Moreover, PA notably increased cyclooxygenase (COX)-2 protein expression, and PA-induced expression of both Bcl-2 and Bcl-xL was inhibited by NS-398, a specific inhibitor of COX-2. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 142-148 cytochrome c oxidase II, mitochondrial Mus musculus 174-179 17371157-13 2007 NS-398, a selective COX-2 inhibitor, blocked the strontium ranelate stimulation of PGE(2) production and significantly inhibited the strontium ranelate stimulation of ALP activity. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 0-6 cytochrome c oxidase II, mitochondrial Mus musculus 20-25 15893191-6 2005 Cardioprotection and increases in PGE2 and 6-keto-PGF(1-alpha) were completely abolished by the COX-2-selective inhibitor NS-398 and the non-selective COX inhibitor indomethacin, whereas the COX-1-selective inhibitor SC-560 had no effect. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 122-128 cytochrome c oxidase II, mitochondrial Mus musculus 96-101 17351141-3 2007 Since there are no data available so far on the role of COX-2 in the amygdala, in a first step we demonstrated that the selective COX-2 inhibitor NS-398 significantly reduced the probability of long-term potentiation (LTP) induction in the lateral nucleus of the amygdala. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 146-152 cytochrome c oxidase II, mitochondrial Mus musculus 56-61 17351141-3 2007 Since there are no data available so far on the role of COX-2 in the amygdala, in a first step we demonstrated that the selective COX-2 inhibitor NS-398 significantly reduced the probability of long-term potentiation (LTP) induction in the lateral nucleus of the amygdala. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 146-152 cytochrome c oxidase II, mitochondrial Mus musculus 130-135 16962108-7 2006 Vehicle alone or NS398 (a selective COX-2 inhibitor, 10 mg/kg of weight per day) were administered orally daily for 56 days after implantation. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 17-22 cytochrome c oxidase II, mitochondrial Mus musculus 36-41 16960384-6 2006 Consistently, NS-398, a COX-2 inhibitor, stimulated TNF-alpha-induced apoptosis, which was reversed by exogenous PGE2 and PGF 2alpha. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 14-20 cytochrome c oxidase II, mitochondrial Mus musculus 24-29 16892182-6 2006 In addition, a selective COX-2 inhibitor, NS-398, significantly inhibited the increased cAMP level induced by BFT stimulation. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 42-48 cytochrome c oxidase II, mitochondrial Mus musculus 25-30 15947245-8 2005 The inhibitor of cyclooxygenase-1 (COX-1), SC-560, did not affect the basal tone of arterioles, whereas NS-398, an inhibitor of COX-2, caused a significant shift in the arteriolar pressure-diameter curve of vessels from db/db mice (at 80 mm Hg, 76+/-3%) but not in those of control mice. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 104-110 cytochrome c oxidase II, mitochondrial Mus musculus 128-133 17303115-7 2007 Intraperitoneal administration of indomethacin (20 mg/kg), a non-specific COX inhibitor, or NS-398 (10 mg/kg), a specific COX-2 inhibitor, impaired performance on the retention trial in the task, while piroxicam (20 mg/kg), a specific COX-1 inhibitor, did not. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 92-98 cytochrome c oxidase II, mitochondrial Mus musculus 122-127 17762187-6 2007 Inhibition of MIN6 cell COX2 activity with a selective inhibitor, NS-398 (10-100 microM), increased apoptosis and exogenous PGE(2) (0.2-5 microM) reduced NS-398-induced apoptosis in a concentration-dependent manner. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 66-72 cytochrome c oxidase II, mitochondrial Mus musculus 24-28 17762187-6 2007 Inhibition of MIN6 cell COX2 activity with a selective inhibitor, NS-398 (10-100 microM), increased apoptosis and exogenous PGE(2) (0.2-5 microM) reduced NS-398-induced apoptosis in a concentration-dependent manner. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 154-160 cytochrome c oxidase II, mitochondrial Mus musculus 24-28 16532483-3 2006 We report that indomethacin, a nonspecific inhibitor of COX, and NS398, a specific inhibitor of COX2, preserved muscle mass and reduced type 1 TNF receptors in muscles of mice bearing the Lewis lung carcinoma, but not in mice bearing the B16 melanoma. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 65-70 cytochrome c oxidase II, mitochondrial Mus musculus 96-100 16418805-6 2006 with 100 mug COX-2 selective inhibitors (LM01, LM08, LM11, and NS398), on every other day from day 0 to 30, significantly reduced the incidence and severity of EAE in SJL/J and C57BL/6 mice. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 63-68 cytochrome c oxidase II, mitochondrial Mus musculus 13-18 15925391-6 2005 The non-selective cyclooxygenase (COX) inhibitor diclofenac and the selective COX-2 inhibitors NS-398 and JTE-522 dose dependently reduced the acute herpetic pain, and NS-398 was without effect on delayed postherpetic pain. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 95-101 cytochrome c oxidase II, mitochondrial Mus musculus 78-83 15925391-6 2005 The non-selective cyclooxygenase (COX) inhibitor diclofenac and the selective COX-2 inhibitors NS-398 and JTE-522 dose dependently reduced the acute herpetic pain, and NS-398 was without effect on delayed postherpetic pain. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 168-174 cytochrome c oxidase II, mitochondrial Mus musculus 78-83 15850932-7 2005 Specific COX-2 inhibition with NS398 lowered brain PGE2 levels by about 60%. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 31-36 cytochrome c oxidase II, mitochondrial Mus musculus 9-14 15721291-6 2005 COX-2 was induced in Adv-C/EBPbeta-infected hepatocytes, and the addition of NS398, a specific inhibitor of COX-2, suppressed the viability-maintenance effect. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 77-82 cytochrome c oxidase II, mitochondrial Mus musculus 0-5 15721291-6 2005 COX-2 was induced in Adv-C/EBPbeta-infected hepatocytes, and the addition of NS398, a specific inhibitor of COX-2, suppressed the viability-maintenance effect. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 77-82 cytochrome c oxidase II, mitochondrial Mus musculus 108-113 15358864-7 2004 These effects were reversed by NS398, a COX-2-specific inhibitor, suggesting that lipopolysaccharide-mediated inhibition of CUGBP2 is a PG-dependent mechanism. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 31-36 cytochrome c oxidase II, mitochondrial Mus musculus 40-45 15797258-5 2005 The PGE2 production induced by either AEA or MAEA was completely inhibited by NS-398, a selective cyclooxygenase (COX)-2 inhibitor, suggesting that COX-2 was induced. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 78-84 cytochrome c oxidase II, mitochondrial Mus musculus 98-120 15797258-5 2005 The PGE2 production induced by either AEA or MAEA was completely inhibited by NS-398, a selective cyclooxygenase (COX)-2 inhibitor, suggesting that COX-2 was induced. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 78-84 cytochrome c oxidase II, mitochondrial Mus musculus 148-153 15576468-7 2005 On the other hand, two highly selective inhibitors for COX-2, NS-398 (N-[2-(cyclohexyloxy)-4-nitrophenyl]-methanesulfonamide) and CAY10404 [3-(4-methylsulphonylphenyl)-4-phenyl-5-trifluoromethylisoxazole], dose-dependently inhibited both adhesion formation and the increase in PGE2 levels (3-30 mg/kg). N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 62-68 cytochrome c oxidase II, mitochondrial Mus musculus 55-60 15576468-7 2005 On the other hand, two highly selective inhibitors for COX-2, NS-398 (N-[2-(cyclohexyloxy)-4-nitrophenyl]-methanesulfonamide) and CAY10404 [3-(4-methylsulphonylphenyl)-4-phenyl-5-trifluoromethylisoxazole], dose-dependently inhibited both adhesion formation and the increase in PGE2 levels (3-30 mg/kg). N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 70-124 cytochrome c oxidase II, mitochondrial Mus musculus 55-60 15168734-6 2004 This effect was abrogated by the selective Cox-2 inhibitor NS-398, and by the anti-inflammatory glucocorticoid dexamethasone. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 59-65 cytochrome c oxidase II, mitochondrial Mus musculus 43-48 14760389-4 2004 NS-398 (100 microM), a highly selective COX-2 inhibitor, decreased cell proliferation by approximately 35% of control, as determined using [(3)H]-thymidine incorporation. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 0-6 cytochrome c oxidase II, mitochondrial Mus musculus 40-45 14698956-8 2003 Considering that these doses of NS-398 had no significant effect on cellular proliferation or cell cycle distribution in C3H 10T1/2 cells, the results suggest that inhibition of COX-2 either increases DNA repair or prevents the accumulation of DNA damage. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 32-38 cytochrome c oxidase II, mitochondrial Mus musculus 178-183 12865315-6 2003 Although SC560, a selective COX1 inhibitor, did not affect steroidogenesis, the COX2 inhibitor NS398 significantly enhanced Bt(2)cAMP-stimulated StAR protein expression and steroid production. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 95-100 cytochrome c oxidase II, mitochondrial Mus musculus 80-84 14563940-4 2003 In this model, VEGF expression was down-regulated by selective COX-2 inhibition with NS-398. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 85-91 cytochrome c oxidase II, mitochondrial Mus musculus 63-68 14563940-7 2003 S-180 cells implanted in ddy mice formed substantial tumors with extensive angiogenesis markedly suppressed by aspirin and COX-2 inhibitors NS-398 and JTE522, but not by mofezolac, an inhibitor of constitutive COX-1. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 140-146 cytochrome c oxidase II, mitochondrial Mus musculus 123-128 12505683-1 2003 This study was designed to investigate the time lag of effect of NS398, selective COX-2 inhibitor, on infarct volume and neurologic deficits in mice with experimentally-induced cerebral ischemia. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 65-70 cytochrome c oxidase II, mitochondrial Mus musculus 82-87 12433932-4 2003 However, in the present study we found that both piroxicam, a general COX inhibitor, and NS-398, a COX-2 selective inhibitor, effectively suppressed the activation of transcription factor activator protein 1 (AP-1) induced by ultraviolet B (UVB) or 12-O-tetradecanoylphorbol-13-acetate in mouse epidermal JB6 cells. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 89-95 cytochrome c oxidase II, mitochondrial Mus musculus 99-104 12401438-4 2002 The effect of NS-398 on lipid body formation was independent of its inhibitory effects on COX-2 since arachidonate-induced lipid body formation in COX-2-deficient mouse leukocytes was also inhibited by NS-398. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 14-20 cytochrome c oxidase II, mitochondrial Mus musculus 147-152 12360491-7 2002 Treatment with NS-398 (a COX-2 inhibitor) significantly decreased the severity of pancreatitis. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 15-21 cytochrome c oxidase II, mitochondrial Mus musculus 25-30 12401438-4 2002 The effect of NS-398 on lipid body formation was independent of its inhibitory effects on COX-2 since arachidonate-induced lipid body formation in COX-2-deficient mouse leukocytes was also inhibited by NS-398. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 202-208 cytochrome c oxidase II, mitochondrial Mus musculus 147-152 12401438-5 2002 By means of its ability to inhibit leukocyte lipid body formation, NS-398 may exert actions independent of its COX-2 inhibition and more broadly contribute to the suppression of formation of COX-1 and lipoxygenase-derived eicosanoids. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 67-73 cytochrome c oxidase II, mitochondrial Mus musculus 111-116 12088417-0 2001 The COX-2 inhibitor NS-398 causes T-cell developmental disruptions independent of COX-2 enzyme inhibition. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 20-26 cytochrome c oxidase II, mitochondrial Mus musculus 4-9 11788337-7 2002 The COX-2 inhibitor NS-398 suppressed PGE(2) production and normalized IL-12 production in the injury group, whereas it had no effect on IL-10 production. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 20-26 cytochrome c oxidase II, mitochondrial Mus musculus 4-9 12124326-5 2002 We also examined the tumoricidal effectiveness of combining PDT with the selective COX-2 inhibitor NS-398. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 99-105 cytochrome c oxidase II, mitochondrial Mus musculus 83-88 11982590-3 2002 NS398, a specific COX-2 inhibitor, and indomethacin (IM), a COX-1 and COX-2 inhibitor, enhanced viable BCG-induced cytotoxic activity and IFN-gamma and TNF-alpha production of PEC. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 0-5 cytochrome c oxidase II, mitochondrial Mus musculus 18-23 12088417-6 2001 We focused on the NS-398 COX-2 inhibitor and showed that its effects could not be reversed by exogenous PGE2. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 18-24 cytochrome c oxidase II, mitochondrial Mus musculus 25-30 12088417-7 2001 Furthermore, NS-398 was inhibitory even when its target, COX-2, was absent. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 13-19 cytochrome c oxidase II, mitochondrial Mus musculus 57-62 11504678-3 2001 We observed a significant time-dependent upregulation of PGE(2) production in both blood and lung homogenates of mice administered lipopolysaccharide intraperitoneally, which was nearly completely suppressed by the administration of the COX-2 inhibitor NS-398. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 253-259 cytochrome c oxidase II, mitochondrial Mus musculus 237-242 11770048-6 2001 The mice were treated with the COX-2 inhibitor NS-398 (10 mg/kg body weight, intraperitoneally) or vehicle immediately after trauma-hemorrhage or sham operation, 12 h thereafter, and following CLP or sham CLP. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 47-53 cytochrome c oxidase II, mitochondrial Mus musculus 31-36 11195467-3 2000 The NSAIDs used in this study include acetylsalicylic acid (ASA) that is anti-inflammatory with COX-1 and COX-2 inhibition and N-[2-(cyclohexyloxy)-4-nitrophenyl]-methanesulfonamide (NS398) that is a specific COX-2 inhibitor. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 127-181 cytochrome c oxidase II, mitochondrial Mus musculus 209-214 11477553-5 2001 PGE(2) production by C3L5 cells was primarily owing to COX-2, since this was blocked similarly with non-selective COX inhibitor indomethacin and selective COX-2 inhibitor NS-398, but unaffected with the selective COX-1 inhibitor valeryl salicylate. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 171-177 cytochrome c oxidase II, mitochondrial Mus musculus 55-60 11444591-4 2001 NS-398, a specific COX-2 inhibitor, inhibited leptin release by 27% in adipose tissue from control mice, 31% in tissue from COX-1-/- mice and by 23% in tissue from COX-2+/- mice while having no effect on leptin release by adipose tissue from COX-2-/- mice. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 0-6 cytochrome c oxidase II, mitochondrial Mus musculus 19-24 11444591-4 2001 NS-398, a specific COX-2 inhibitor, inhibited leptin release by 27% in adipose tissue from control mice, 31% in tissue from COX-1-/- mice and by 23% in tissue from COX-2+/- mice while having no effect on leptin release by adipose tissue from COX-2-/- mice. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 0-6 cytochrome c oxidase II, mitochondrial Mus musculus 164-169 11444591-4 2001 NS-398, a specific COX-2 inhibitor, inhibited leptin release by 27% in adipose tissue from control mice, 31% in tissue from COX-1-/- mice and by 23% in tissue from COX-2+/- mice while having no effect on leptin release by adipose tissue from COX-2-/- mice. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 0-6 cytochrome c oxidase II, mitochondrial Mus musculus 164-169 11414733-4 2001 For lipopolysaccharide (LPS)-treated BM-DC, inhibition of PGE(2) production by indomethacin or by NS-398 (a COX-2-selective inhibitor) used alone was less potent. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 98-104 cytochrome c oxidase II, mitochondrial Mus musculus 108-113 11351503-8 2001 On the other hand, Cd at 1 microM and above stimulated PGE2 production and its production was inhibited by an inhibitor of COX-2 (NS-398). N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 130-136 cytochrome c oxidase II, mitochondrial Mus musculus 123-128 11368536-2 2001 We hypothesize that blocking PGE(2) with NS-398, a selective COX-2 inhibitor, will modulate this response and improve outcome. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 41-47 cytochrome c oxidase II, mitochondrial Mus musculus 61-66 11368536-11 2001 NS-398 treatment also attenuated COX-2 mRNA levels and NF-kappaB activation. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 0-6 cytochrome c oxidase II, mitochondrial Mus musculus 33-38 11195467-7 2000 ASA (294 mg/kg diet) and NS398 also inhibited the expression of COX-2. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 25-30 cytochrome c oxidase II, mitochondrial Mus musculus 64-69 11028559-3 2000 We hypothesized that blocking PGE2 with NS-398, a selective COX-2 inhibitor, during the first 24 h after injury may modify the immune response and protect the host from a subsequent septic challenge. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 40-46 cytochrome c oxidase II, mitochondrial Mus musculus 60-65 10773026-4 2000 In segments of colon mounted in Ussing chambers, arachidonic acid caused a concentration-dependent increase in short-circuit current that was blocked by piroxicam, the COX-2 inhibitor NS-398, and the COX-1 inhibitor SC-560. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 184-190 cytochrome c oxidase II, mitochondrial Mus musculus 168-173 10873667-3 2000 We report here that administration of the selective COX-2 inhibitor NS-398 prevents the onset of diabetes in mice brought on by multiple low-doses of streptozotocin (STZ). N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 68-74 cytochrome c oxidase II, mitochondrial Mus musculus 52-57 10773011-7 2000 Similar results were obtained with the specific COX-2 inhibitor NS-398 (10-30 microM) but not with the selective COX-1 inhibitor valeryl salicylate (10-300 microM). N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 64-70 cytochrome c oxidase II, mitochondrial Mus musculus 48-53 10864883-5 2000 NS-398 (a selective COX-2 inhibitor) reduced LPS plus UTP-elicited iNOS induction and nitrite accumulation, supporting for the positive regulation of iNOS gene expression by endogenous PGE(2). N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 0-6 cytochrome c oxidase II, mitochondrial Mus musculus 20-25 10607728-3 2000 A differential inhibition was found with N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide, a selective inhibitor of the cyclooxygenase isoenzyme COX-2: the promoting effect of TPA, but not that of TCDD, was abolished. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 41-92 cytochrome c oxidase II, mitochondrial Mus musculus 148-153 10541284-5 1999 When COX enzyme activity was measured in the M-1 cells, both indomethacin (COX-1 and -2 inhibitor) and the specific COX-2 inhibitor NS-398 effectively blocked PGE2 synthesis. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 132-138 cytochrome c oxidase II, mitochondrial Mus musculus 116-121 10541284-7 1999 By Western blot analysis, COX-2 expression was significantly upregulated by incubation with either indomethacin or NS-398. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 115-121 cytochrome c oxidase II, mitochondrial Mus musculus 26-31 10463387-11 1999 The cox-2-selective inhibitors NS-398 and DFU and the less selective inhibitor meloxicam, potently impeded Cd-induced Ca release (IC50 of 1 nM, 41 nM and 7 nM, respectively) and calvarial production of PGE2. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 31-37 cytochrome c oxidase II, mitochondrial Mus musculus 4-9 10376946-6 1999 This induction was time- and concentration-dependent, and prevented by inhibitors of transcription and translation, as well as the selective COX-2 inhibitor, NS-398. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 158-164 cytochrome c oxidase II, mitochondrial Mus musculus 141-146 9535546-6 1998 A second COX-2 inhibitor, NS 398 (0.1, 1, 10 mg/kg), was dosed p.o. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 26-32 cytochrome c oxidase II, mitochondrial Mus musculus 9-14 34580604-8 2021 PP2, PDTC, or COX-2 inhibitor NS-398 ameliorated abnormal proliferation and expression of fibrotic proteins induced by HG. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 30-36 cytochrome c oxidase II, mitochondrial Mus musculus 14-19 9031736-26 1997 In comparative experiments indomethacin, a non selective COX inhibitor, and NS-398, a selective COX-2 inhibitor, reduced (LPS) stimulated 6-keto-PGF1alpha production in J774 macrophages in a dose-dependent manner without affecting nitrite release. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 76-82 cytochrome c oxidase II, mitochondrial Mus musculus 96-101 34511032-10 2022 However, PAR2 activation did not induce COX-2 expression in CMT-93 cells and inhibition of COX-2 by COX-2 selective inhibitor (NS-398) did not alter PAR2-induced wound healing. N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 127-133 cytochrome c oxidase II, mitochondrial Mus musculus 91-96