PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 31039577-12 2019 Additionally, a combination treatment strategy of low-dose aspirin given concomitantly with a selective COX-2 inhibitor may result in a reduced side effect profile compared to aspirin or selective COX-2 inhibitor use alone. Aspirin 59-66 mitochondrially encoded cytochrome c oxidase II Homo sapiens 104-109 30701538-1 2019 Several clinical studies indicated that the daily use of aspirin or acetylsalicylic acid reduces the cancer risk via cyclooxygenases (Cox-1 and Cox-2) inhibition. Aspirin 57-64 mitochondrially encoded cytochrome c oxidase II Homo sapiens 144-149 30701538-1 2019 Several clinical studies indicated that the daily use of aspirin or acetylsalicylic acid reduces the cancer risk via cyclooxygenases (Cox-1 and Cox-2) inhibition. Aspirin 68-88 mitochondrially encoded cytochrome c oxidase II Homo sapiens 144-149 30737317-9 2019 Nonsteroidal anti-inflammatory drugs (e.g. aspirin, ibuprofen, and naproxen) block PG synthesis by inhibiting COX-1 and COX-2. Aspirin 43-50 mitochondrially encoded cytochrome c oxidase II Homo sapiens 120-125 31039577-12 2019 Additionally, a combination treatment strategy of low-dose aspirin given concomitantly with a selective COX-2 inhibitor may result in a reduced side effect profile compared to aspirin or selective COX-2 inhibitor use alone. Aspirin 59-66 mitochondrially encoded cytochrome c oxidase II Homo sapiens 197-202 31039577-12 2019 Additionally, a combination treatment strategy of low-dose aspirin given concomitantly with a selective COX-2 inhibitor may result in a reduced side effect profile compared to aspirin or selective COX-2 inhibitor use alone. Aspirin 176-183 mitochondrially encoded cytochrome c oxidase II Homo sapiens 104-109 30096040-0 2019 Residual cyclooxygenase activity of aspirin-acetylated COX-2 forms 15 R-prostaglandins that inhibit platelet aggregation. Aspirin 36-43 mitochondrially encoded cytochrome c oxidase II Homo sapiens 55-60 30096040-6 2019 Aspirin increased 15 R-PGD2 but not 15 R-PGE2 in isolated human leukocytes activated with LPS to induce COX-2. Aspirin 0-7 mitochondrially encoded cytochrome c oxidase II Homo sapiens 104-109 30096040-9 2019 15 R-PGs are novel products of aspirin therapy via acetylation of COX-2 and may contribute to its antiplatelet and other pharmacologic effects.-Gimenez-Bastida, J. Aspirin 31-38 mitochondrially encoded cytochrome c oxidase II Homo sapiens 66-71 30096040-10 2019 A., Boeglin, W. E., Boutaud, O., Malkowski, M. G., Schneider, C. Residual cyclooxygenase activity of aspirin-acetylated COX-2 forms 15 R-prostaglandins that inhibit platelet aggregation. Aspirin 101-108 mitochondrially encoded cytochrome c oxidase II Homo sapiens 120-125 30106307-9 2018 Also, it possessed better affinity value, -7.80518 kcal/mol and energy binding -85.08 kcal/mol, in inhibition of COX-2 with PDB Id: 1CVU rather than other compounds and significantly the higher dock score than aspirin, close to celecoxib. Aspirin 210-217 mitochondrially encoded cytochrome c oxidase II Homo sapiens 113-118 29982425-4 2018 Under in vitro conditions, NO-Aspirin significantly reduced the proliferation and survival of tumorigenic bronchial cell line (1170) and non-small cell lung cancer (NSCLC) cell lines (A549, H1650, H1975 and HCC827) and colony formation by NSCLC cells at sub- or low micromolar concentrations (<=1 microM for 1170 cells and <=6 microM for NSCLC cells) in a COX-2 independent manner. Aspirin 30-37 mitochondrially encoded cytochrome c oxidase II Homo sapiens 362-367 29552221-3 2018 In the prostaglandin-dependent pathways, inhibition of cyclooxygenase (COX), particularly COX-2, is the primary mechanism known to be involved in aspirin-induced CRC suppression. Aspirin 146-153 mitochondrially encoded cytochrome c oxidase II Homo sapiens 90-95 28948649-0 2018 Association of GPIa and COX-2 gene polymorphism with aspirin resistance. Aspirin 53-60 mitochondrially encoded cytochrome c oxidase II Homo sapiens 24-29 28948649-1 2018 OBJECTIVE: This study aimed to explore the association between GPIa, COX-2 gene polymorphisms and aspirin resistance in the ischemic stroke patients from the southern part of Jiangsu province. Aspirin 98-105 mitochondrially encoded cytochrome c oxidase II Homo sapiens 69-74 29316620-2 2018 Aspirin is the most commonly used non-steroid anti-inflammatory drugs (NSAIDs), and it irreversibly inhibits cyclooxygenase-1 and -2 (COX1, COX2). Aspirin 0-7 mitochondrially encoded cytochrome c oxidase II Homo sapiens 140-144 29316620-4 2018 The lower aspirin doses causing only minimal gastrointestinal disturbance, ideal for long-term use, can achieve only partial and transitory inhibition of COX2. Aspirin 10-17 mitochondrially encoded cytochrome c oxidase II Homo sapiens 154-158 29316620-5 2018 Aspirin"s principal metabolite, salicylic acid, is also found in fruits and vegetables that inhibit COX2. Aspirin 0-7 mitochondrially encoded cytochrome c oxidase II Homo sapiens 100-104 28346830-7 2017 A combination of DHA and ASA efficiently enhanced heterodimer formations of PPARalpha and RXRalpha and increased the expression of neurotrophic factors PSD-95, brain-derived neurotrophic factor (BDNF), and glial cell-derived neurotrophic factor (GDNF), while inhibiting NFkappaB and COX2. Aspirin 25-28 mitochondrially encoded cytochrome c oxidase II Homo sapiens 283-287 27405497-9 2017 Clinical data on aspirin, an irreversible inhibitor of both COX-1 and COX-2, are mainly experimental and hypothetical at this stage, but may be promising in depressed patients with concomitant inflammatory conditions. Aspirin 17-24 mitochondrially encoded cytochrome c oxidase II Homo sapiens 70-75 28344655-0 2017 Interactions among COX-2, GPIIIa and P2Y1 variants are associated with aspirin responsiveness and adverse events in patients with ischemic stroke. Aspirin 71-78 mitochondrially encoded cytochrome c oxidase II Homo sapiens 19-24 28051316-5 2017 Compounds 6 and 7A inhibited COX-2 by 10% and 8%, respectively, at a concentration of 12.5 muM compared to 12% for 1 mM aspirin (the positive control). Aspirin 120-127 mitochondrially encoded cytochrome c oxidase II Homo sapiens 29-34 28068952-0 2017 Interaction among COX-2, P2Y1 and GPIIIa gene variants is associated with aspirin resistance and early neurological deterioration in Chinese stroke patients. Aspirin 74-81 mitochondrially encoded cytochrome c oxidase II Homo sapiens 18-23 27887602-1 2016 It has been suggested that aspirin may be of benefit in treating sepsis and ARDS in view of its ability to block cyclo-oxygenase-1 (COX-1) and COX-2 activities; inhibit nuclear factor kappa B (NF-kappaB); enhance the production of endothelial nitric oxide (eNO) and lipoxin A4 (LXA4). Aspirin 27-34 mitochondrially encoded cytochrome c oxidase II Homo sapiens 143-148 26859324-5 2016 We determined the crystal structures of S530T murine (mu) COX-2, aspirin-acetylated human (hu) COX-2, and huCOX-2 in complex with salicylate to 1.9, 2.0, and 2.4 A, respectively. Aspirin 65-72 mitochondrially encoded cytochrome c oxidase II Homo sapiens 95-100 27344083-7 2016 The aspirin-mediated inactivation of platelets may restore antitumor reactivity by blocking the release of paracrine lipid and protein mediators that induce COX-2 expression in adjacent nucleated cells at sites of mucosal injury. Aspirin 4-11 mitochondrially encoded cytochrome c oxidase II Homo sapiens 157-162 27489545-1 2016 In subjects with non-steroidal anti-inflammatory drugs (NSAIDs)- exacerbated respiratory disease (NERD) symptoms are triggered by acetyl salicylic acid (ASA) and other strong COX-1 inhibitors, and in some cases by weak COX-1 or by selective COX-2 inhibitors. Aspirin 153-156 mitochondrially encoded cytochrome c oxidase II Homo sapiens 241-246 26980433-4 2016 The expression of COX2 mRNA in platelets and its influences on the effect of aspirin was also investigated. Aspirin 77-84 mitochondrially encoded cytochrome c oxidase II Homo sapiens 18-22 26859324-1 2016 Aspirin and other nonsteroidal anti-inflammatory drugs target the cyclooxygenase enzymes (COX-1 and COX-2) to block the formation of prostaglandins. Aspirin 0-7 mitochondrially encoded cytochrome c oxidase II Homo sapiens 100-105 27318652-0 2016 Interaction between COX-1 and COX-2 Variants Associated with Aspirin Resistance in Chinese Stroke Patients. Aspirin 61-68 mitochondrially encoded cytochrome c oxidase II Homo sapiens 30-35 26859324-7 2016 On the basis of these structural observations, along with functional analysis of the S530T/G533V double mutant, we propose a working hypothesis for the generation of 15R-HETE by aspirin-acetylated COX-2. Aspirin 178-185 mitochondrially encoded cytochrome c oxidase II Homo sapiens 197-202 26254051-6 2015 However, there is cross-reactivity between the NSAIDs in patients with NSAID-exacerbated cutaneous disease and NIUA, and thus only use of selective COX-2 inhibitors can replace the culprit drug if the chronic treatment is necessary, although aspirin desensitization will allow for chronic treatment with NSAIDs in some patients with NIUA. Aspirin 242-249 mitochondrially encoded cytochrome c oxidase II Homo sapiens 148-153 26201059-6 2015 Acetylation of COX-2 allows for generation of 15-(R)HETE and subsequent formation of "aspirin-triggered lipoxin" (ATL) by interaction with white cell lipoxygenases. Aspirin 86-93 mitochondrially encoded cytochrome c oxidase II Homo sapiens 15-20 26085050-6 2015 For example, aspirin at antiplatelet doses might acetylate COX-2 in vascular cells, directing the activity of the enzyme into a 15-lipoxygenase which by transcellular metabolism results in the formation of 15-epi-lipoxin ( aspirin-triggered lipoxin ), an antiinflammatory mediator. Aspirin 13-20 mitochondrially encoded cytochrome c oxidase II Homo sapiens 59-64 26085050-6 2015 For example, aspirin at antiplatelet doses might acetylate COX-2 in vascular cells, directing the activity of the enzyme into a 15-lipoxygenase which by transcellular metabolism results in the formation of 15-epi-lipoxin ( aspirin-triggered lipoxin ), an antiinflammatory mediator. Aspirin 223-230 mitochondrially encoded cytochrome c oxidase II Homo sapiens 59-64 26560040-0 2016 Low E-prostanoid 2 receptor levels and deficient induction of the IL-1beta/IL-1 type I receptor/COX-2 pathway: Vicious circle in patients with aspirin-exacerbated respiratory disease. Aspirin 143-150 mitochondrially encoded cytochrome c oxidase II Homo sapiens 96-101 26560040-1 2016 BACKGROUND: We hypothesized that the 2 reported alterations in aspirin-exacerbated respiratory disease (AERD), reduced expression/production of COX-2/prostaglandin (PG) E2 and diminished expression of E-prostanoid (EP) 2 receptor, are closely linked. Aspirin 63-70 mitochondrially encoded cytochrome c oxidase II Homo sapiens 144-149 26319435-5 2015 Since the parent compound aspirin, inhibits both COX-1 and COX-2, we also evaluated the effects of these compounds on COX-1 and COX-2 enzyme activities and also performed modeling of the interactions between the positional isomers of NOSH-aspirin and COX-1 and COX-2 enzymes. Aspirin 26-33 mitochondrially encoded cytochrome c oxidase II Homo sapiens 59-64 26319435-10 2015 All 3 positional isomers of NOSH-aspirin preferentially inhibited COX-1 over COX-2. Aspirin 33-40 mitochondrially encoded cytochrome c oxidase II Homo sapiens 77-82 25380191-8 2015 This review synthesizes the evidence on the COX-2-independent mechanisms of action of aspirin, salicylates, and other NSAIDs on breast cancer. Aspirin 86-93 mitochondrially encoded cytochrome c oxidase II Homo sapiens 44-49 25239119-8 2015 Besides, the survival benefit of postdiagnosis aspirin use appeared to be confined to those patients with positive prostaglandin endoperoxide synthase 2 (PTGS2, also known as cyclooxygenase-2, COX-2) expression (HR=0.65, 95% CI 0.50 to 0.85) and with mutated PIK3CA tumours (HR=0.58, 95% CI 0.37 to 0.90). Aspirin 47-54 mitochondrially encoded cytochrome c oxidase II Homo sapiens 193-198 25239119-11 2015 CONCLUSIONS: These findings provide further indication that postdiagnosis aspirin therapy improved CRC overall survival, especially for patients with positive PTGS2 (COX-2) expression and mutated PIK3CA tumours. Aspirin 74-81 mitochondrially encoded cytochrome c oxidase II Homo sapiens 166-171 25638779-3 2015 Aspirin (acetylsalicylate, ASA) inhibits AA oxidation by cyclooxygenase (COX)-1 and COX-2. Aspirin 0-7 mitochondrially encoded cytochrome c oxidase II Homo sapiens 84-89 25638779-3 2015 Aspirin (acetylsalicylate, ASA) inhibits AA oxidation by cyclooxygenase (COX)-1 and COX-2. Aspirin 9-25 mitochondrially encoded cytochrome c oxidase II Homo sapiens 84-89 25638779-3 2015 Aspirin (acetylsalicylate, ASA) inhibits AA oxidation by cyclooxygenase (COX)-1 and COX-2. Aspirin 27-30 mitochondrially encoded cytochrome c oxidase II Homo sapiens 84-89 24388008-0 2014 Safety risks for patients with aspirin-exacerbated respiratory disease after acute exposure to selective nonsteroidal anti-inflammatory drugs and COX-2 inhibitors: Meta-analysis of controlled clinical trials. Aspirin 31-38 mitochondrially encoded cytochrome c oxidase II Homo sapiens 146-151 26137580-0 2015 COX-2 and EGFR: Partners in Crime Split by Aspirin. Aspirin 43-50 mitochondrially encoded cytochrome c oxidase II Homo sapiens 0-5 25759598-4 2015 All available NSAIDs, including acetaminophen and aspirin, are associated with potential side effects, particularly gastrointestinal and cardiovascular effects, related to their relative selectivity for COX-1 and COX-2. Aspirin 50-57 mitochondrially encoded cytochrome c oxidase II Homo sapiens 213-218 25967073-8 2015 Walls of ruptured human intracranial aneurysms have higher levels of COX-2 and microsomal prostaglandin E2 synthase 1 (mPGES-1), both of which are known to be inhibited by aspirin. Aspirin 172-179 mitochondrially encoded cytochrome c oxidase II Homo sapiens 69-74 25967073-9 2015 In a pilot study, patients undergoing microsurgical clipping had attenuated expression of COX-2, mPGES-1, and macrophages in aneurysm walls after 3 months of aspirin therapy versus those that did not receive aspirin. Aspirin 158-165 mitochondrially encoded cytochrome c oxidase II Homo sapiens 90-95 25967073-11 2015 Treatment with aspirin also resulted in decreased expression of COX-2 within leukocytes within aneurysms as compared to peripheral blood samples. Aspirin 15-22 mitochondrially encoded cytochrome c oxidase II Homo sapiens 64-69 26369678-3 2015 Epidemiological, clinical, and observational studies have demonstrated that aspirin and non-steroidal antiinflammatory drugs (NSAIDs), including COX-2 inhibitors, can protect against CRC and significantly reduce its incidence. Aspirin 76-83 mitochondrially encoded cytochrome c oxidase II Homo sapiens 145-150 25666703-6 2015 In contrast to native NSAIDs, their NO-releasing derivatives such as NO-ASA were found to exhibit lower gastric toxicity despite inhibiting both COX-1 and COX-2 activity in the gastric mucosa. Aspirin 72-75 mitochondrially encoded cytochrome c oxidase II Homo sapiens 155-160 24796340-10 2014 Our results suggest that a genetic decrease in COX-2 activity may be beneficial with respect to CVD risk, especially, in higher risk patients on aspirin. Aspirin 145-152 mitochondrially encoded cytochrome c oxidase II Homo sapiens 47-52 25006185-10 2014 Among aspirin users, concomitant selective cox-2 inhibitor use was no longer associated with increased hazard for cardiovascular events. Aspirin 6-13 mitochondrially encoded cytochrome c oxidase II Homo sapiens 43-48 25085874-3 2014 Therefore, we examined the association between recent (1 year) prediagnostic use of aspirin (COX1/COX2 inhibitor), lymph node involvement at breast cancer diagnosis, and breast cancer-specific mortality. Aspirin 84-91 mitochondrially encoded cytochrome c oxidase II Homo sapiens 98-102 24953043-1 2014 Aspirin (ASA) is a commonly used nonsteroidal anti-inflammatory drug (NSAID), which exerts its therapeutic effects through inhibition of cyclooxygenase (COX) isoform 2 (COX-2), while the inhibition of COX-1 by ASA leads to apparent side effects. Aspirin 0-7 mitochondrially encoded cytochrome c oxidase II Homo sapiens 169-174 24953043-1 2014 Aspirin (ASA) is a commonly used nonsteroidal anti-inflammatory drug (NSAID), which exerts its therapeutic effects through inhibition of cyclooxygenase (COX) isoform 2 (COX-2), while the inhibition of COX-1 by ASA leads to apparent side effects. Aspirin 9-12 mitochondrially encoded cytochrome c oxidase II Homo sapiens 169-174 24953043-1 2014 Aspirin (ASA) is a commonly used nonsteroidal anti-inflammatory drug (NSAID), which exerts its therapeutic effects through inhibition of cyclooxygenase (COX) isoform 2 (COX-2), while the inhibition of COX-1 by ASA leads to apparent side effects. Aspirin 210-213 mitochondrially encoded cytochrome c oxidase II Homo sapiens 169-174 25093007-21 2014 Taking an aspirin (ASA) regularly after being diagnosed with colon cancer is associated with less risk of dying from this cancer, especially among people who have tumors with COX-2 overexpression.16 Nonetheless, these data do not contradict the data obtained on a possible genetic predisposition, even in sporadic or non-hereditary CRC. Aspirin 10-17 mitochondrially encoded cytochrome c oxidase II Homo sapiens 175-180 25093007-21 2014 Taking an aspirin (ASA) regularly after being diagnosed with colon cancer is associated with less risk of dying from this cancer, especially among people who have tumors with COX-2 overexpression.16 Nonetheless, these data do not contradict the data obtained on a possible genetic predisposition, even in sporadic or non-hereditary CRC. Aspirin 19-22 mitochondrially encoded cytochrome c oxidase II Homo sapiens 175-180 24783984-6 2014 Special emphasis is given to the ability of aspirin to acetylate cyclooxygenases (especially COX-2) and thus to initiate a biochemical pathway leading to the generation of anti-inflammatory pro-resolving mediators synthesized from both omega-3 and omega-6 long-chain polyunsaturated fatty acids. Aspirin 44-51 mitochondrially encoded cytochrome c oxidase II Homo sapiens 93-98 24503478-8 2014 The cyclooxygenase activity of nanodisc-reconstituted COX-2 was reduced by aspirin acetylation and potentiated by the nonsubstrate fatty acid palmitic acid to the same extent as detergent solubilized enzyme, independent of phospholipid composition. Aspirin 75-82 mitochondrially encoded cytochrome c oxidase II Homo sapiens 54-59 24520038-7 2014 For aspirin, the major mechanism is the anti-inflammatory action through the inhibition of COX-1/COX-2 and modulation of the NFkappaB or STAT3 pathway. Aspirin 4-11 mitochondrially encoded cytochrome c oxidase II Homo sapiens 97-102 24605250-7 2014 Daily low-dose aspirin achieves complete and persistent inhibition of cyclooxygenase (COX)-1 in platelets (in pre-systemic circulation) while causing a limited and rapidly reversible inhibitory effect on COX-2 and/or COX-1 expressed in nucleated cells. Aspirin 15-22 mitochondrially encoded cytochrome c oxidase II Homo sapiens 204-209 24327271-4 2014 In these cohorts, the survival benefit of aspirin was shown to depend upon the level of COX-2 expression in the primary colorectal cancer. Aspirin 42-49 mitochondrially encoded cytochrome c oxidase II Homo sapiens 88-93 24327271-6 2014 Aspirin intake following colorectal cancer resection was associated with a significant improvement of survival in patients whose tumors carried mutant, but not wild-type, copies of the phosphoinositide 3-kinase (PI3KCA) gene, especially tumors that overexpressed COX-2. Aspirin 0-7 mitochondrially encoded cytochrome c oxidase II Homo sapiens 263-268 23810915-1 2013 BACKGROUND: Studies have examined whether tumor expression of PTGS2 (also known as COX-2), an enzyme inhibited by nonsteroidal anti-inflammatory drugs such as aspirin, is associated with prognosis in patients with colorectal cancer. Aspirin 159-166 mitochondrially encoded cytochrome c oxidase II Homo sapiens 83-88 23723142-9 2014 Moreover, safety concerns related to alternative medications such as acetaminophen and selective COX-2 inhibitors may influence users of these drugs to switch to aspirin and NSAIDs. Aspirin 162-169 mitochondrially encoded cytochrome c oxidase II Homo sapiens 97-102 24244288-10 2013 CONCLUSION: Our findings provide strong evidence that COX-2 and ITGA2 genetic defects might increase the risk of having aspirin insensitivity, especially for aspirin semi-resistance and in Chinese populations. Aspirin 120-127 mitochondrially encoded cytochrome c oxidase II Homo sapiens 54-59 24244288-10 2013 CONCLUSION: Our findings provide strong evidence that COX-2 and ITGA2 genetic defects might increase the risk of having aspirin insensitivity, especially for aspirin semi-resistance and in Chinese populations. Aspirin 158-165 mitochondrially encoded cytochrome c oxidase II Homo sapiens 54-59 24209633-0 2014 Aspirin inhibits lipopolysaccharide-induced COX-2 expression and PGE2 production in porcine alveolar macrophages by modulating protein kinase C and protein tyrosine phosphatase activity. Aspirin 0-7 mitochondrially encoded cytochrome c oxidase II Homo sapiens 44-49 24209633-1 2014 Aspirin has been demonstrated to be effective in inhibiting COX-2 and PGE(2) in Alveolar macrophages (AMs). Aspirin 0-7 mitochondrially encoded cytochrome c oxidase II Homo sapiens 60-65 24209633-3 2014 In the present study, we found that pretreatment with aspirin inhibited LPS-induced COX-2 and PGE(2) upregulation, IkappaBalpha degradation, NFkappaB activation and the increase of PKC activity, but elevated LPS-induced the decrease of PTP activity. Aspirin 54-61 mitochondrially encoded cytochrome c oxidase II Homo sapiens 84-89 24209633-5 2014 Furthermore, the PTP inhibitor mitigated the inhibitory effect of aspirin on COX-2 and PGE(2) upregulation and NF-kappaB activation, whereas the PKC inhibitor enhanced the inhibitory effects of aspirin on the production of COX-2 and PGE(2). Aspirin 66-73 mitochondrially encoded cytochrome c oxidase II Homo sapiens 77-82 24282256-2 2014 Aspirin inhibits several pathways mediated by NF-kappaB, COX-2, or their targets that are important in multiple myeloma pathogenesis. Aspirin 0-7 mitochondrially encoded cytochrome c oxidase II Homo sapiens 57-62 24282256-12 2014 This prospective study of aspirin use and multiple myeloma supports an etiologic role for aspirin-inhibited (i.e., NF-kappaB- or COX-2 mediated) pathways. Aspirin 90-97 mitochondrially encoded cytochrome c oxidase II Homo sapiens 129-134 23786234-2 2013 For COX-2, the stereochemistry and relative abundance of generated products is influenced by Ser530 acetylation following aspirin treatment. Aspirin 122-129 mitochondrially encoded cytochrome c oxidase II Homo sapiens 4-9 22609818-1 2013 BACKGROUND: Cyclooxygenase 1 (COX-1), COX-2, and HO-1 are involved in the process of aspirin"s effect. Aspirin 85-92 mitochondrially encoded cytochrome c oxidase II Homo sapiens 38-43 23786234-3 2013 The molecular bases of the high degree of stereospecificity which characterizes COX-2-catalyzed oxygenations are not yet completely understood, nor are the reasons behind the aspirin-induced shift in lipid mediator production. Aspirin 175-182 mitochondrially encoded cytochrome c oxidase II Homo sapiens 80-85 23786234-5 2013 This hypothesis is supported by a computational model which accurately reproduces experimental oxygenation patterns on both native and aspirin-inhibited COX-2. Aspirin 135-142 mitochondrially encoded cytochrome c oxidase II Homo sapiens 153-158 22001128-4 2012 Since safe aspirin regimens can only achieve a partial and transitory inhibition of cox-2, it may be feasible to complement the cancer-protective benefit of aspirin with other measures which decrease cox-2 expression or which limit the bioactivity of cox-2-derived PGE2. Aspirin 11-18 mitochondrially encoded cytochrome c oxidase II Homo sapiens 84-89 23506529-3 2013 Aspirin is a non-steroidal anti-inflammatory drug that is an irreversible inhibitor of both cyclooxygenase (COX)-1 and COX-2, It stimulates endogenous production of anti-inflammatory regulatory "braking signals", including lipoxins, which dampen the inflammatory response and reduce levels of inflammatory biomarkers, including C-reactive protein, tumor necrosis factor-alpha and interleukin (IL)--6, but not negative immunoregulatory cytokines, such as IL-4 and IL-10. Aspirin 0-7 mitochondrially encoded cytochrome c oxidase II Homo sapiens 119-124 23525414-9 2013 Expression of COX-2 (but not COX-1), mPGES-1, and macrophages was lower in the ASA group than in the control group. Aspirin 79-82 mitochondrially encoded cytochrome c oxidase II Homo sapiens 14-19 24281340-3 2012 At low-doses given every 24 h, aspirin is acting by a complete and persistent inhibition of cyclooxygenase (COX)-1 in platelets (in the pre-systemic circulation) while causing a limited and rapidly reversible inhibitory effect on COX-2 and/or COX-1 expressed in nucleated cells. Aspirin 31-38 mitochondrially encoded cytochrome c oxidase II Homo sapiens 230-235 23668350-4 2013 Furthermore, ibuprofen and aspirin were found to be preferential inhibitor of COX-1 and COX-2, respectively. Aspirin 27-34 mitochondrially encoded cytochrome c oxidase II Homo sapiens 88-93 23401648-2 2013 As the protective effect of aspirin has been associated with an increased expression of COX-2, molecular imaging of COX-2, for instance, during confocal endomicroscopy could enable the identification of patients who would possibly benefit from aspirin treatment. Aspirin 28-35 mitochondrially encoded cytochrome c oxidase II Homo sapiens 88-93 23401648-2 2013 As the protective effect of aspirin has been associated with an increased expression of COX-2, molecular imaging of COX-2, for instance, during confocal endomicroscopy could enable the identification of patients who would possibly benefit from aspirin treatment. Aspirin 28-35 mitochondrially encoded cytochrome c oxidase II Homo sapiens 116-121 23401648-2 2013 As the protective effect of aspirin has been associated with an increased expression of COX-2, molecular imaging of COX-2, for instance, during confocal endomicroscopy could enable the identification of patients who would possibly benefit from aspirin treatment. Aspirin 244-251 mitochondrially encoded cytochrome c oxidase II Homo sapiens 88-93 23401648-2 2013 As the protective effect of aspirin has been associated with an increased expression of COX-2, molecular imaging of COX-2, for instance, during confocal endomicroscopy could enable the identification of patients who would possibly benefit from aspirin treatment. Aspirin 244-251 mitochondrially encoded cytochrome c oxidase II Homo sapiens 116-121 21361874-8 2011 The bcl-2, p53 and cox-2 genes in both cell lines treated with ASA seem to exhibit different patterns of expression. Aspirin 63-66 mitochondrially encoded cytochrome c oxidase II Homo sapiens 19-24 22039321-7 2011 Treatment with NO-ASA dose-dependently accelerated colonic healing followed by a rise in plasma NO(x) content and CBF, suppression of MPO and downregulation of COX-2, iNOS, IL-1beta and TNF-alpha mRNAs. Aspirin 18-21 mitochondrially encoded cytochrome c oxidase II Homo sapiens 160-165 21645153-0 2011 Two novel aspirin analogues show selective cytotoxicity in primary chronic lymphocytic leukaemia cells that is associated with dual inhibition of Rel A and COX-2. Aspirin 10-17 mitochondrially encoded cytochrome c oxidase II Homo sapiens 156-161 21361874-4 2011 The mechanism of action of different concentrations of ASA were compared in K562 (non-MDR) and Lucena (MDR) cells by analysing cell viability, apoptosis and necrosis, intracellular ROS (reactive oxygen species) formation and bcl-2, p53 and cox-2 gene expression. Aspirin 55-58 mitochondrially encoded cytochrome c oxidase II Homo sapiens 240-245 22122764-7 2011 Aspirin and non-aspirin NSAIDs inhibit COX-2, subsequent PGE(2) formation and action by transcriptional and non-transcriptional mechanisms. Aspirin 0-7 mitochondrially encoded cytochrome c oxidase II Homo sapiens 39-44 22122764-7 2011 Aspirin and non-aspirin NSAIDs inhibit COX-2, subsequent PGE(2) formation and action by transcriptional and non-transcriptional mechanisms. Aspirin 16-23 mitochondrially encoded cytochrome c oxidase II Homo sapiens 39-44 22122764-9 2011 Aspirin additionally acetylates COX-2, resulting in generation of "aspirin-triggered" lipoxins (ATL), a new class of anti-inflammatory/antitumour compounds. Aspirin 0-7 mitochondrially encoded cytochrome c oxidase II Homo sapiens 32-37 22122764-9 2011 Aspirin additionally acetylates COX-2, resulting in generation of "aspirin-triggered" lipoxins (ATL), a new class of anti-inflammatory/antitumour compounds. Aspirin 67-74 mitochondrially encoded cytochrome c oxidase II Homo sapiens 32-37 21688627-4 2011 The GI protection that is associated with the use of COX-2 selective agents is largely lost when low-dose aspirin is administered concurrently for CV prophylaxis. Aspirin 106-113 mitochondrially encoded cytochrome c oxidase II Homo sapiens 53-58 20920611-6 2011 Aspirin (ASA) converts cyclooxygenase (COX)-2 into a form that generates new neuroprotective docosanoids from DHA; therefore, ASA might positively resolve the paradoxical effect of the concomitant presence of DHA and betaA. Aspirin 0-7 mitochondrially encoded cytochrome c oxidase II Homo sapiens 23-45 20920611-6 2011 Aspirin (ASA) converts cyclooxygenase (COX)-2 into a form that generates new neuroprotective docosanoids from DHA; therefore, ASA might positively resolve the paradoxical effect of the concomitant presence of DHA and betaA. Aspirin 9-12 mitochondrially encoded cytochrome c oxidase II Homo sapiens 23-45 20920611-6 2011 Aspirin (ASA) converts cyclooxygenase (COX)-2 into a form that generates new neuroprotective docosanoids from DHA; therefore, ASA might positively resolve the paradoxical effect of the concomitant presence of DHA and betaA. Aspirin 126-129 mitochondrially encoded cytochrome c oxidase II Homo sapiens 23-45 21548865-6 2011 This review was designed to provide an updated overview based on the experimental and clinical evidence on the involvement COX-2 derived products, lipoxins in the mechanism of gastric defense, gastroprotection and gastric adaptation to ASA. Aspirin 236-239 mitochondrially encoded cytochrome c oxidase II Homo sapiens 123-128 21548865-9 2011 Aspirin-triggered lipoxin (ATL) synthesis, via COX-2, acts to reduce the severity of damage induced by this NSAID. Aspirin 0-7 mitochondrially encoded cytochrome c oxidase II Homo sapiens 47-52 21548865-12 2011 Suppression of COX-2 activity by selective COX-2 inhibitors such as rofecoxib or celecoxib was shown to abolish the production of ATL and to diminish the gastric tolerability of ASA and gastric adaptation developed in response to repetitive administration of this NSAID. Aspirin 178-181 mitochondrially encoded cytochrome c oxidase II Homo sapiens 15-20 21548865-12 2011 Suppression of COX-2 activity by selective COX-2 inhibitors such as rofecoxib or celecoxib was shown to abolish the production of ATL and to diminish the gastric tolerability of ASA and gastric adaptation developed in response to repetitive administration of this NSAID. Aspirin 178-181 mitochondrially encoded cytochrome c oxidase II Homo sapiens 43-48 20359903-5 2010 Aspirin being a COX-2 inhibitor has been shown to reduce the chance of metastasis in adenocarcinoma but not squamous carcinoma. Aspirin 0-7 mitochondrially encoded cytochrome c oxidase II Homo sapiens 16-21 22022418-8 2011 P-selectin glycoprotein ligand-1 (PSGL-1) blocking antibody, which abrogates MPA formation, abolished these effects, as did the cyclooxygenase (COX)-2 selective inhibitor NS-398, aspirin and the EP1/EP2-selective antagonist AH6809. Aspirin 179-186 mitochondrially encoded cytochrome c oxidase II Homo sapiens 128-150 21542252-5 2011 ATL (AT mean aspirin triggered therefore "depend on aspirin") synthesis, via COX-2, reduces the severity of damage gastrointestinal tract induced by NSAIDs. Aspirin 13-20 mitochondrially encoded cytochrome c oxidase II Homo sapiens 77-82 21542252-5 2011 ATL (AT mean aspirin triggered therefore "depend on aspirin") synthesis, via COX-2, reduces the severity of damage gastrointestinal tract induced by NSAIDs. Aspirin 52-59 mitochondrially encoded cytochrome c oxidase II Homo sapiens 77-82 19706045-9 2009 Aspirin initially caused a time-dependent decrease in COX-2 expression but subsequently, and unexpectedly, elevated the latter. Aspirin 0-7 mitochondrially encoded cytochrome c oxidase II Homo sapiens 54-59 27713316-2 2010 Aspirin and several small molecule NSAIDs are known to inhibit the enzymes cyclooxygenase-1 (COX-1) and -2 (COX-2). Aspirin 0-7 mitochondrially encoded cytochrome c oxidase II Homo sapiens 108-113 20223228-8 2010 Treatment of aspirin significantly prevented the progression of nephropathy and inhibited the augmented COX-2, NFkappaB (p65 levels), TNFalpha, and TGFbeta-smad expression. Aspirin 13-20 mitochondrially encoded cytochrome c oxidase II Homo sapiens 104-109 19880272-0 2010 Aspirin inhibits MMP-9 mRNA expression and release via the PPARalpha/gamma and COX-2/mPGES-1-mediated pathways in macrophages derived from THP-1 cells. Aspirin 0-7 mitochondrially encoded cytochrome c oxidase II Homo sapiens 79-84 19880272-4 2010 Additionally, the COX-2 mRNA expression, mPGES-1 mRNA and protein expression in macrophages were all decreased after incubation with aspirin for 24h and the PGE(2) release was also decreased. Aspirin 133-140 mitochondrially encoded cytochrome c oxidase II Homo sapiens 18-23 19880272-7 2010 It might be concluded that aspirin could inhibit the MMP-9 gene expression and release through the PPARalpha/gamma and COX-2/mPGES-1-mediated pathways and the two pathways might be partly overlapped and even be interrelated. Aspirin 27-34 mitochondrially encoded cytochrome c oxidase II Homo sapiens 119-124 20631416-2 2010 The elucidation by John Vane of the mechanism of action of aspirin in 1971 was followed twenty years later by the discovery of a second cyclooxygenase enzyme, COX-2 and the rapid development of selective inhibitors of this enzyme. Aspirin 59-66 mitochondrially encoded cytochrome c oxidase II Homo sapiens 159-164 20631416-3 2010 The COX-2 inhibitors are potent anti-inflammatory drugs without the damaging side effects on the stomach mucosa of the non-selective aspirin-like inhibitors. Aspirin 133-140 mitochondrially encoded cytochrome c oxidase II Homo sapiens 4-9 20233202-0 2010 Aspirin-triggered lipoxin in patients treated with aspirin and selective vs. nonselective COX-2 inhibitors. Aspirin 0-7 mitochondrially encoded cytochrome c oxidase II Homo sapiens 90-95 20233202-2 2010 We tested the hypothesis that the co-administration of aspirin with either the selective COX-2 inhibitor celecoxib or the nonselective COX inhibitor ibuprofen reduces ATL biosynthesis. Aspirin 55-62 mitochondrially encoded cytochrome c oxidase II Homo sapiens 89-94 20648923-9 2010 Furthermore, compared to ASA and to diclofenac (Diclo, CAS 15307-79-6), the COX-1 and COX-2 mRNA expressions were influenced differently by STW 33-I and fraction E. ASA and Diclo inhibited both the COX-1 and COX-2 mRNA expressions, whereas STW 33-I and its fraction E increased the COX-1 mRNA expression. Aspirin 165-168 mitochondrially encoded cytochrome c oxidase II Homo sapiens 86-91 20648923-9 2010 Furthermore, compared to ASA and to diclofenac (Diclo, CAS 15307-79-6), the COX-1 and COX-2 mRNA expressions were influenced differently by STW 33-I and fraction E. ASA and Diclo inhibited both the COX-1 and COX-2 mRNA expressions, whereas STW 33-I and its fraction E increased the COX-1 mRNA expression. Aspirin 165-168 mitochondrially encoded cytochrome c oxidase II Homo sapiens 208-213 19706045-10 2009 Stimulation of COX-2 expression by aspirin was further enhanced following stimulation of the Wnt/beta-catenin pathway. Aspirin 35-42 mitochondrially encoded cytochrome c oxidase II Homo sapiens 15-20 19706045-11 2009 Application of the COX-2 inhibitor NS-398 suppressed elevated COX-2 expression and promoted aspirin-induced apoptosis. Aspirin 92-99 mitochondrially encoded cytochrome c oxidase II Homo sapiens 19-24 19563267-2 2009 The common anti-inflammatory drugs (such as aspirin, ibuprofen and naproxen) all act by blocking the action of both the COX-1 and COX-2 enzymes. Aspirin 44-51 mitochondrially encoded cytochrome c oxidase II Homo sapiens 130-135 19576865-5 2009 COX-2 expression was induced by p-NO-ASA, protein kinase C inhibitors reversed this induction. Aspirin 37-40 mitochondrially encoded cytochrome c oxidase II Homo sapiens 0-5 19680014-3 2009 Inhibition of cyclooxygenase (COX)-1 and COX-2 by aspirin or its related compounds, nonsteroidal antiinflammatory drugs (NSAIDs), has been associated with both adverse and beneficial effects in the gastrointestinal (GI) tract. Aspirin 50-57 mitochondrially encoded cytochrome c oxidase II Homo sapiens 41-46 19680014-11 2009 Inhibition of COX-2 by NSAIDs, coxibs, or aspirin seems to provide beneficial effects to the GI tract. Aspirin 42-49 mitochondrially encoded cytochrome c oxidase II Homo sapiens 14-19 19493461-15 2009 Aspirin decreased COX-2 expression in a dose-dependent manner at mRNA and protein levels. Aspirin 0-7 mitochondrially encoded cytochrome c oxidase II Homo sapiens 18-23 19534809-11 2009 Both of these markers were increased upon COX-2 suppression by aspirin pretreatment prior to DCA exposure. Aspirin 63-70 mitochondrially encoded cytochrome c oxidase II Homo sapiens 42-47 19601807-5 2009 Metabolites of 15-LOX-1 and 2 are anti-tumorigenic; similarly, 15-epi-LXA(4) synthesized during COX-2 acetylation by low doses of aspirin too possesses anti-tumorigenic effects. Aspirin 130-137 mitochondrially encoded cytochrome c oxidase II Homo sapiens 96-101 19601807-6 2009 Acetylating nonsteroidal anti-inflammatory drugs (NSAIDs), like aspirin, switches COX-2 from forming PGE(2) (promoting tumorigenesis) to 15-epi-LXA(4) (antitumorigenesis). Aspirin 64-71 mitochondrially encoded cytochrome c oxidase II Homo sapiens 82-87 18812631-8 2008 Aspirin-triggered lipoxin synthesis, via COX-2, acts to reduce the severity of damage induced by this drug. Aspirin 0-7 mitochondrially encoded cytochrome c oxidase II Homo sapiens 41-46 19236238-3 2009 Conversely, NSAIDs including aspirin inhibit COX-2 and, therefore, have anti-neoplastic properties. Aspirin 29-36 mitochondrially encoded cytochrome c oxidase II Homo sapiens 45-50 18805632-8 2009 When COX-2 expression was knocked down using siRNA against cox-2, the expression of p21(cip-1) was induced by NO-ASA, regardless of the level of expression of COX-2, suggesting a marginal, if any, role for COX-2 in the growth inhibitory effect of NO-ASA. Aspirin 113-116 mitochondrially encoded cytochrome c oxidase II Homo sapiens 5-10 18805632-8 2009 When COX-2 expression was knocked down using siRNA against cox-2, the expression of p21(cip-1) was induced by NO-ASA, regardless of the level of expression of COX-2, suggesting a marginal, if any, role for COX-2 in the growth inhibitory effect of NO-ASA. Aspirin 113-116 mitochondrially encoded cytochrome c oxidase II Homo sapiens 59-64 18805632-8 2009 When COX-2 expression was knocked down using siRNA against cox-2, the expression of p21(cip-1) was induced by NO-ASA, regardless of the level of expression of COX-2, suggesting a marginal, if any, role for COX-2 in the growth inhibitory effect of NO-ASA. Aspirin 250-253 mitochondrially encoded cytochrome c oxidase II Homo sapiens 5-10 18805632-8 2009 When COX-2 expression was knocked down using siRNA against cox-2, the expression of p21(cip-1) was induced by NO-ASA, regardless of the level of expression of COX-2, suggesting a marginal, if any, role for COX-2 in the growth inhibitory effect of NO-ASA. Aspirin 250-253 mitochondrially encoded cytochrome c oxidase II Homo sapiens 59-64 19345936-5 2009 Herein, we tested a variety of Cox-1/Cox-2 non-selective NSAIDs, namely ibuprofen, tylenol, aspirin and naproxen and report that they blunt IgM and IgG synthesis in stimulated human peripheral blood mononuclear cells (PBMC). Aspirin 92-99 mitochondrially encoded cytochrome c oxidase II Homo sapiens 37-42 19938885-0 2009 Low-dose aspirin reduces gastro-protective properties of COX-2 selective inhibitors. Aspirin 9-16 mitochondrially encoded cytochrome c oxidase II Homo sapiens 57-62 19938885-2 2009 With this case we emphasize that the potential of the stomach-protecting properties of COX-2 selective inhibitors may be reduced in patients who are simultaneously taking aspirin. Aspirin 171-178 mitochondrially encoded cytochrome c oxidase II Homo sapiens 87-92 19938885-3 2009 We also review several pathogenic mechanisms that have been advanced by animal studies to explain the finding that a COX-2 selective inhibitor plus low-dose aspirin leads to an ulcer rate near that of a dual COX-1/COX-2 inhibitor alone. Aspirin 157-164 mitochondrially encoded cytochrome c oxidase II Homo sapiens 214-219 19114773-7 2009 COX-2 inhibition still seems preferred option, as the effects observed with aspirin (the only chemopreventive agent with some apparent future) are more profound only in tumors and cells expressing COX-2. Aspirin 76-83 mitochondrially encoded cytochrome c oxidase II Homo sapiens 0-5 19114773-7 2009 COX-2 inhibition still seems preferred option, as the effects observed with aspirin (the only chemopreventive agent with some apparent future) are more profound only in tumors and cells expressing COX-2. Aspirin 76-83 mitochondrially encoded cytochrome c oxidase II Homo sapiens 197-202 19114773-10 2009 By inhibiting COX-2 or other tumorigenic targets, NSAIDs, especially aspirin or new aspirin derivates, may prevent colon cancer in selected populations. Aspirin 69-76 mitochondrially encoded cytochrome c oxidase II Homo sapiens 14-19 19114773-10 2009 By inhibiting COX-2 or other tumorigenic targets, NSAIDs, especially aspirin or new aspirin derivates, may prevent colon cancer in selected populations. Aspirin 84-91 mitochondrially encoded cytochrome c oxidase II Homo sapiens 14-19 21701610-10 2009 Acetylsalicylic acid appears to diminish the benefit of COX-2s over tNSAIDs. Aspirin 0-20 mitochondrially encoded cytochrome c oxidase II Homo sapiens 56-61 18753249-2 2008 Clinical data show that mixed COX-1/COX-2 inhibitors such as aspirin, but not COX-2 selective inhibitors such as rofecoxib, induce bronchoconstriction and asthma in sensitive individuals. Aspirin 61-68 mitochondrially encoded cytochrome c oxidase II Homo sapiens 36-41 18753249-8 2008 Cells cultured from aspirin-sensitive or control human donors contained similar levels of COX-1 and COX-2 immunoreactivity. Aspirin 20-27 mitochondrially encoded cytochrome c oxidase II Homo sapiens 100-105 19575683-5 2009 Patients with aspirin sensitivity are often able to tolerate selective COX-2 inhibitors. Aspirin 14-21 mitochondrially encoded cytochrome c oxidase II Homo sapiens 71-76 18053020-1 2008 BACKGROUND AND AIMS: Aspirin, a cyclo-oxygenase (COX)-1 and COX-2 inhibitor, is the antiplatelet drug of choice to prevent serious vascular events. Aspirin 21-28 mitochondrially encoded cytochrome c oxidase II Homo sapiens 60-65 18090373-9 2008 The COX-1 and COX-2 inhibitor aspirin (10(-6)-10(-5) mol/L) and the COX-2 inhibitor nimesulide (10(-6) mol/L) induced leftward shifts of the concentration-response curve for vasopressin in gastroepiploic artery. Aspirin 30-37 mitochondrially encoded cytochrome c oxidase II Homo sapiens 14-19 17584993-15 2008 Thus, PGE2 is released during the clinical reactions to aspirin through an alternative COX-2 pathway. Aspirin 56-63 mitochondrially encoded cytochrome c oxidase II Homo sapiens 87-92 17584993-16 2008 The clinical implications of this finding are in line with current observations of good tolerance of the selective COX-2 inhibitors in aspirin-sensitive patients. Aspirin 135-142 mitochondrially encoded cytochrome c oxidase II Homo sapiens 115-120 18156036-10 2007 Data support the conclusion that COX-2 inhibitors are preferable to non-selective NSAIDs in patients with chronic pain and cardiovascular risk needing low-dose aspirin, but relative risks and benefits should be assessed individually for each patient. Aspirin 160-167 mitochondrially encoded cytochrome c oxidase II Homo sapiens 33-38 17339623-8 2007 Colorectal adenoma incidence was also reduced with non-ASA NSAID use in cohort studies (relative risk, 0.64 [CI, 0.48 to 0.85]) and case-control studies (relative risk, 0.54 [CI, 0.4 to 0.74]) and by COX-2 inhibitors in randomized, controlled trials (relative risk, 0.72 [CI, 0.68 to 0.77]). Aspirin 55-58 mitochondrially encoded cytochrome c oxidase II Homo sapiens 200-205 18034968-11 2007 Several studies have indicated that selective COX-2 inhibitors can be safely administered in patients with aspirin-exacerbated respiratory disease and NSAID-induced cutaneous reactions, although their use has been curtailed by their cardiovascular side effects. Aspirin 107-114 mitochondrially encoded cytochrome c oxidase II Homo sapiens 46-51 17609236-13 2007 However, approximately 4% of patients with a history of aspirin-induced skin reactions may experience a cutaneous reaction following a challenge to a COX-2 selective NSAID. Aspirin 56-63 mitochondrially encoded cytochrome c oxidase II Homo sapiens 150-155 17609236-15 2007 CONCLUSIONS: Management of patients with aspirin/NSAID sensitivity includes avoidance of aspirin/nonselective NSAIDs, use of COX-2 selective NSAIDs, acetaminophen in doses less than 1000 mg, and desensitization. Aspirin 41-48 mitochondrially encoded cytochrome c oxidase II Homo sapiens 125-130 17556027-10 2007 The co-administration of acetylsalicylic acid appears to reduce the GI safety of COX-2s in subgroup analyses. Aspirin 25-45 mitochondrially encoded cytochrome c oxidase II Homo sapiens 81-86 17556027-12 2007 The co-administration of acetylsalicylic acid might reduce the safety advantage of COX-2s over that of nonselective NSAIDs. Aspirin 25-45 mitochondrially encoded cytochrome c oxidase II Homo sapiens 83-88 17485013-5 2007 RESULTS: The COX-1 and COX-2 inhibitor aspirin at high concentrations (10(-6) to 10(-5) mol/L) and the COX-2 inhibitor nimesulide (10(-6) mol/L) potentiated the contractile responses of the arterial rings to sympathetic neurogenic stimulation and norepinephrine. Aspirin 39-46 mitochondrially encoded cytochrome c oxidase II Homo sapiens 23-28 17485013-9 2007 Aspirin at high concentrations and the COX-2 selective inhibitor nimesulide potentiated the contractile response of gastroepiploic artery to adrenergic stimulation by inhibiting COX-2-derived PGI(2). Aspirin 0-7 mitochondrially encoded cytochrome c oxidase II Homo sapiens 178-183 18064329-9 2007 Evolutionary, this mechanism may prevent COX-2-dependent thromboxane synthesis in the platelet, which would potentiate the likelihood of thrombosis; pharmacologically, this mechanism would prevent an aspirin-insensitive pathway of thromboxane formation. Aspirin 200-207 mitochondrially encoded cytochrome c oxidase II Homo sapiens 41-46 17978563-7 2007 The selective inhibition index on COX-2, IC(50) (COX-1)/IC(50) (COX-2), of Cu-Asp was 3.33+/-0.89, while that of Asp was 0.42+/-0.12. Aspirin 78-81 mitochondrially encoded cytochrome c oxidase II Homo sapiens 34-39 17978563-7 2007 The selective inhibition index on COX-2, IC(50) (COX-1)/IC(50) (COX-2), of Cu-Asp was 3.33+/-0.89, while that of Asp was 0.42+/-0.12. Aspirin 78-81 mitochondrially encoded cytochrome c oxidase II Homo sapiens 64-69 17978563-8 2007 The results suggest that, unlike Asp, Cu-Asp is a relatively selective inhibitor of COX-2 in the present models; the selectivity of Cu-Asp is about seven-fold greater than that of Asp. Aspirin 41-44 mitochondrially encoded cytochrome c oxidase II Homo sapiens 84-89 17609236-12 2007 COX-2 selective NSAIDs, especially in patients with aspirin-induced asthma, have not been found to cross-react. Aspirin 52-59 mitochondrially encoded cytochrome c oxidase II Homo sapiens 0-5 19075973-6 2007 The common anti-inflammatory drugs (like aspirin, ibuprofen, and naproxen) all act by blocking the action of both the COX-1 and COX-2 enzymes. Aspirin 41-48 mitochondrially encoded cytochrome c oxidase II Homo sapiens 128-133 17136297-9 2006 Selective COX 2 inhibitors can be prescribed in some cases of allergy to aspirin, but they must be used with care. Aspirin 73-80 mitochondrially encoded cytochrome c oxidase II Homo sapiens 10-15 17016059-2 2007 BACKGROUND: The anti-inflammatory actions of acetylsalicylic acid (ASA)/non-steroidal anti-inflammatory drugs (NSAIDs) are thought to be due to inhibition of COX-2, whereas the side effects such as gastric damage and aspirin-induced asthma are mediated through inhibition of COX-1. Aspirin 45-65 mitochondrially encoded cytochrome c oxidase II Homo sapiens 158-163 17016059-2 2007 BACKGROUND: The anti-inflammatory actions of acetylsalicylic acid (ASA)/non-steroidal anti-inflammatory drugs (NSAIDs) are thought to be due to inhibition of COX-2, whereas the side effects such as gastric damage and aspirin-induced asthma are mediated through inhibition of COX-1. Aspirin 67-70 mitochondrially encoded cytochrome c oxidase II Homo sapiens 158-163 17016059-3 2007 Therefore, a new class of drugs with COX-2 selectivity may be well tolerated by patients with ASA/NSAIDs hypersensitivity. Aspirin 94-97 mitochondrially encoded cytochrome c oxidase II Homo sapiens 37-42 17319904-0 2007 Reticulated platelets and uninhibited COX-1 and COX-2 decrease the antiplatelet effects of aspirin. Aspirin 91-98 mitochondrially encoded cytochrome c oxidase II Homo sapiens 48-53 17319904-2 2007 Immature (reticulated) platelets may modulate the antiplatelet effects of aspirin through uninhibited cyclooxygenase (COX)-1 and COX-2. Aspirin 74-81 mitochondrially encoded cytochrome c oxidase II Homo sapiens 129-134 17168813-6 2006 It is very well known that pain and inflammation are alleviated through the inhibition of COX-2 inhibitors such as Aspirin, which has resulted in the recent years, in the emergence of a range of COX-2 inhibitors. Aspirin 115-122 mitochondrially encoded cytochrome c oxidase II Homo sapiens 90-95 17168813-6 2006 It is very well known that pain and inflammation are alleviated through the inhibition of COX-2 inhibitors such as Aspirin, which has resulted in the recent years, in the emergence of a range of COX-2 inhibitors. Aspirin 115-122 mitochondrially encoded cytochrome c oxidase II Homo sapiens 195-200 16859832-5 2006 COX-1 and COX-2 inhibition by traditional NSAIDs (for example, aspirin) although chemopreventive have some side effects due to the role of COX-1 in maintaining the integrity of the gastric mucosa. Aspirin 63-70 mitochondrially encoded cytochrome c oxidase II Homo sapiens 10-15 16952320-4 2006 Aspirin is an inhibitor of COX-2 and has been implicated, with other non-steroidal anti-inflammatory drugs (NSAIDS) in prevention and treatment of breast cancer. Aspirin 0-7 mitochondrially encoded cytochrome c oxidase II Homo sapiens 27-32 16960142-3 2006 Epilipoxins, for instance, are produced from aspirin"s acetylation of COX-2 and together with Resolvins and COX-2-derived prostaglandins of the D(2) and J(2) series represent an increasingly important family of immunoregulatory lipid mediators with strong implications for disease control and drug discovery. Aspirin 45-52 mitochondrially encoded cytochrome c oxidase II Homo sapiens 70-75 16519515-1 2006 The two cyclooxygenase enzymes, COX-1 and COX-2, are responsible for the committed step in prostaglandin biosynthesis and are the targets of the nonsteroidal antiinflammatory drugs aspirin and ibuprofen and the COX-2 selective inhibitors, Celebrex, Vioxx, and Bextra. Aspirin 181-188 mitochondrially encoded cytochrome c oxidase II Homo sapiens 42-47 16618538-3 2006 NS398, and ASA, can inhibit PGE2 generation via COX-2 inhibition. Aspirin 11-14 mitochondrially encoded cytochrome c oxidase II Homo sapiens 48-53 16519515-1 2006 The two cyclooxygenase enzymes, COX-1 and COX-2, are responsible for the committed step in prostaglandin biosynthesis and are the targets of the nonsteroidal antiinflammatory drugs aspirin and ibuprofen and the COX-2 selective inhibitors, Celebrex, Vioxx, and Bextra. Aspirin 181-188 mitochondrially encoded cytochrome c oxidase II Homo sapiens 211-216 17181859-3 2006 We hypothesized that genetic polymorphisms (COX-2 .926, COX-2 .5209, and COX-2 .8473) may reduce overall breast cancer risk or risk for subtypes of breast cancer by modulating the inflammatory response and may interact with aspirin or any NSAID use. Aspirin 224-231 mitochondrially encoded cytochrome c oxidase II Homo sapiens 44-49 17181859-3 2006 We hypothesized that genetic polymorphisms (COX-2 .926, COX-2 .5209, and COX-2 .8473) may reduce overall breast cancer risk or risk for subtypes of breast cancer by modulating the inflammatory response and may interact with aspirin or any NSAID use. Aspirin 224-231 mitochondrially encoded cytochrome c oxidase II Homo sapiens 56-61 17181859-3 2006 We hypothesized that genetic polymorphisms (COX-2 .926, COX-2 .5209, and COX-2 .8473) may reduce overall breast cancer risk or risk for subtypes of breast cancer by modulating the inflammatory response and may interact with aspirin or any NSAID use. Aspirin 224-231 mitochondrially encoded cytochrome c oxidase II Homo sapiens 56-61 16395396-6 2006 Among the questions that remain to be addressed are the following: (a) whether this hazard extends to all or some of the traditional NSAIDs; (b) whether adjuvant therapies, such as low-dose aspirin, will mitigate the hazard and if so, at what cost; (c) whether COX-2 inhibitors result in cardiovascular risk transformation during chronic dosing; and (d) how we might identify individuals most likely to benefit or suffer from such drugs in the future. Aspirin 190-197 mitochondrially encoded cytochrome c oxidase II Homo sapiens 261-266 16869344-4 2006 Furthermore, concomitant aspirin use substantially reduces the gastrointestinal safety advantage of COX-2-selective drugs. Aspirin 25-32 mitochondrially encoded cytochrome c oxidase II Homo sapiens 100-105 17154669-7 2006 Selective COX-2 inhibitors (celecoxib and rofecoxib [withdrawn from the market]) are well tolerated by almost all aspirin-sensitive asthmatic patients. Aspirin 114-121 mitochondrially encoded cytochrome c oxidase II Homo sapiens 10-15 16190133-3 2005 On the other hand, aspirin blocks both COX-1 and COX-2 enzymes without decreasing PGI2 but blocks TXA2 synthesis that explains its beneficial action in the prevention of coronary heart disease (CHD). Aspirin 19-26 mitochondrially encoded cytochrome c oxidase II Homo sapiens 49-54 16336399-7 2005 Aspirin dose-dependently decreased the levels of COX-2 mRNA, COX-2 protein and nuclear NF-kappaB protein and increased the cytoplasmic IkappaB protein. Aspirin 0-7 mitochondrially encoded cytochrome c oxidase II Homo sapiens 49-54 16336399-7 2005 Aspirin dose-dependently decreased the levels of COX-2 mRNA, COX-2 protein and nuclear NF-kappaB protein and increased the cytoplasmic IkappaB protein. Aspirin 0-7 mitochondrially encoded cytochrome c oxidase II Homo sapiens 61-66 16227351-2 2005 Selective COX-2 inhibitors were seen as successor to non-selective non-steroidal anti-inflammatory drugs, in turn successors to aspirin. Aspirin 128-135 mitochondrially encoded cytochrome c oxidase II Homo sapiens 10-15 16184416-3 2005 Aspirin induces and acetylates COX-2 to produce 15-(R)-epi-lipoxinA4, an anti-inflammatory mediator thought to protect the gastric mucosa against aspirin-induced injury. Aspirin 0-7 mitochondrially encoded cytochrome c oxidase II Homo sapiens 31-36 16184416-3 2005 Aspirin induces and acetylates COX-2 to produce 15-(R)-epi-lipoxinA4, an anti-inflammatory mediator thought to protect the gastric mucosa against aspirin-induced injury. Aspirin 146-153 mitochondrially encoded cytochrome c oxidase II Homo sapiens 31-36 15978791-2 2005 Originally, the beneficial effects of aspirin were shown to stem from its inhibition of cyclooxygenase (COX 2)-derived prostanoids, fatty acid metabolites that modulate host defense and regulate the cardiovascular system. Aspirin 38-45 mitochondrially encoded cytochrome c oxidase II Homo sapiens 104-109 15978791-4 2005 Here, data from a series of comparatively recent experiments exploring aspirin"s unique ability to acetylate the active site of inducible COX 2 and generate a family of lipid mediators called the epi-Lipoxins will be discussed in light of their ability to exert profound modulatory effects on the innate and adaptive immune systems. Aspirin 71-78 mitochondrially encoded cytochrome c oxidase II Homo sapiens 138-143 16024242-3 2005 Indeed, suppression of aspirin-triggered lipoxin synthesis, through co-administration of a selective COX-2 inhibitor, results in a significant exacerbation of gastric injury. Aspirin 23-30 mitochondrially encoded cytochrome c oxidase II Homo sapiens 101-106 16006977-0 2005 Aspirin, ibuprofen, and other non-steroidal anti-inflammatory drugs in cancer prevention: a critical review of non-selective COX-2 blockade (review). Aspirin 0-7 mitochondrially encoded cytochrome c oxidase II Homo sapiens 125-130 15967068-3 2005 Skin reactions triggered by aspirin are associated with the inhibition of cyclooxygenase, specifically COX-1, but not COX-2, and are characterized by overproduction of cysteinyl leukotrienes (cys-LTs). Aspirin 28-35 mitochondrially encoded cytochrome c oxidase II Homo sapiens 118-123 16190133-4 2005 The inhibitory action of aspirin on COX-1 and COX-2 enzymes enhances the tissue concentrations of dihomo-gamma-linolenic acid (DGLA), arachidonic acid, eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA). Aspirin 25-32 mitochondrially encoded cytochrome c oxidase II Homo sapiens 46-51 15861417-5 2005 RESULTS: Aspirin inhibited constitutive NF-kappaB activity in culture and, in turn, decreased the expression of the NF-kappaB downstream target gene, Cox-2, in PANC-1 or PANC-1/Puro cells, without significantly inhibiting the in vitro growth of PANC-1/Puro cells. Aspirin 9-16 mitochondrially encoded cytochrome c oxidase II Homo sapiens 150-155 15990700-2 2005 In contrast, aspirin blocks both COX-1 and COX-2 enzymes that, in turn, increases intracellular concentrations of dihomo-gamma-linolenic acid (DGLA), arachidonic acid (AA), eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) and reduced formation of eicosanoids. Aspirin 13-20 mitochondrially encoded cytochrome c oxidase II Homo sapiens 43-48 15696570-1 2005 OBJECTIVE: To evaluate the effects of cardiovascular comorbidities and aspirin coprescription on cyclooxygenase (COX)-2 inhibitor (coxib) prescribing patterns among rheumatologists. Aspirin 71-78 mitochondrially encoded cytochrome c oxidase II Homo sapiens 97-119 15921208-2 2005 We hypothesize that Cox-2 also might be relevant in the etiology of nasal polyps of aspirin-tolerant patients by their effects on inflammatory mediators as well as on microvascular permeability. Aspirin 84-91 mitochondrially encoded cytochrome c oxidase II Homo sapiens 20-25 15604423-11 2005 Moreover, the Cox-2 -765C variant displayed a slightly higher reduction in 11-dTxB2 level on treatment with aspirin. Aspirin 108-115 mitochondrially encoded cytochrome c oxidase II Homo sapiens 14-19 15563357-6 2004 Final results of the celecoxib outcome study (CLASS study) attenuated the initial enthusiasm about the GI safety of selective COX-2 inhibitors, especially in patients concomitantly taking aspirin for cardiovascular prophylaxis. Aspirin 188-195 mitochondrially encoded cytochrome c oxidase II Homo sapiens 126-131 15489888-1 2004 Nonsteroidal anti-inflammatory drugs (NSAIDs) such as aspirin have been shown to suppress transcription factor NF-kappaB, which controls the expression of genes such as cyclooxygenase (COX)-2 and cyclin D1, leading to inhibition of proliferation of tumor cells. Aspirin 54-61 mitochondrially encoded cytochrome c oxidase II Homo sapiens 169-191 16168077-4 2005 However, some or all of the gastrointestinal benefit of COX-2 inhibitors may be lost in patients who receive low, cardioprotective doses of aspirin, and recent evidence suggests that some of these agents, at some doses, may be associated with an increased risk for cardiovascular adverse events compared with no therapy. Aspirin 140-147 mitochondrially encoded cytochrome c oxidase II Homo sapiens 56-61 15813652-3 2005 COX-2 inhibitors increase the risk of serious gastroduodenal adverse reactions but there is evidence that they carry a lower risk for these adverse effects than standard NSAIDs, except when there is concurrent aspirin use. Aspirin 210-217 mitochondrially encoded cytochrome c oxidase II Homo sapiens 0-5 16415488-3 2005 Traditional nonsteroidal antiinflammatory drugs (tNSAIDs) and COX-2 inhibitors (coxibs) give rise to antipyretic, analgesic, and antiinflammatory actions, through their reversible clogging of the COX channel of COX-2 - apart from aspirin which modifies irreversibly the catalytic activity of COX-2. Aspirin 230-237 mitochondrially encoded cytochrome c oxidase II Homo sapiens 62-67 15544595-3 2004 We hypothesized that this polymorphism, which may result in decreased COX-2 transcription, could be associated with more severe asthma, and/or aspirin-intolerant asthma (AIA). Aspirin 143-150 mitochondrially encoded cytochrome c oxidase II Homo sapiens 70-75 15297470-1 2004 Administration of selective and nonselective cyclooxygenase (COX)-2 inhibitors to rheumatoid arthritis patients taking low doses of acetylsalicylic acid (ASA) for cardiovascular prevention associates with increased risk of gastrointestinal bleeding. Aspirin 132-152 mitochondrially encoded cytochrome c oxidase II Homo sapiens 45-67 15297470-1 2004 Administration of selective and nonselective cyclooxygenase (COX)-2 inhibitors to rheumatoid arthritis patients taking low doses of acetylsalicylic acid (ASA) for cardiovascular prevention associates with increased risk of gastrointestinal bleeding. Aspirin 154-157 mitochondrially encoded cytochrome c oxidase II Homo sapiens 45-67 15576013-7 2004 It is plausible that the COX-2 inhibition is associated with altered homeostasis that is compensated with the cardioprotection effect of COX-1 inhibition that patients receive either through the less COX-2 selectivity of other NSAIDs or through co-administration of low dose aspirin. Aspirin 275-282 mitochondrially encoded cytochrome c oxidase II Homo sapiens 25-30 15576013-10 2004 However, based on some available indirect evidence, and unless more clear-cut data become available, the use of highly COX-2 selective NSAIDs without the use of a suitable COX-1 inhibitor, (e.g., low dose aspirin) may be best avoided. Aspirin 205-212 mitochondrially encoded cytochrome c oxidase II Homo sapiens 119-124 15163023-1 2004 Cyclooxygenase (COX)-2, the recently described inducible form ofcyclooxygenase, has been shown to be responsible for the inflammatory and tumorigenic effects of prostaglandins; hence the development and expanding clinical use of COX-2 selective inhibitors termed super aspirins. Aspirin 269-277 mitochondrially encoded cytochrome c oxidase II Homo sapiens 0-22 15329003-8 2004 CONCLUSIONS: According to these results the cross-reactivity between aspirin and these COX-2 inhibitors does not occur in subjects with previous respiratory pseudoallergic reactions. Aspirin 69-76 mitochondrially encoded cytochrome c oxidase II Homo sapiens 87-92 14762100-2 2004 Acetylation of COX-2 by aspirin activates a transcellular biosynthetic pathway that switches eicosanoid biosynthesis from prostaglandin E(2) to 15-epi-lipoxin (LX)A(4) or aspirin-triggered lipoxin (ATL). Aspirin 24-31 mitochondrially encoded cytochrome c oxidase II Homo sapiens 15-20 14762100-2 2004 Acetylation of COX-2 by aspirin activates a transcellular biosynthetic pathway that switches eicosanoid biosynthesis from prostaglandin E(2) to 15-epi-lipoxin (LX)A(4) or aspirin-triggered lipoxin (ATL). Aspirin 171-178 mitochondrially encoded cytochrome c oxidase II Homo sapiens 15-20 15480320-0 2004 Dynamics of COX-2 in nasal mucosa and nasal polyps from aspirin-tolerant and aspirin-intolerant patients with asthma. Aspirin 56-63 mitochondrially encoded cytochrome c oxidase II Homo sapiens 12-17 15480320-0 2004 Dynamics of COX-2 in nasal mucosa and nasal polyps from aspirin-tolerant and aspirin-intolerant patients with asthma. Aspirin 77-84 mitochondrially encoded cytochrome c oxidase II Homo sapiens 12-17 15623076-6 2004 Finally, in patients with high cardiovascular risk who should receive a COX-2 selective NSAID, the association with a low dose of acetylsalicylic acid is recommended in order to benefit of a protective antiplatelet effect. Aspirin 130-150 mitochondrially encoded cytochrome c oxidase II Homo sapiens 72-77 15335302-6 2004 New evidence suggests that selective COX-2 inhibitors may be tolerated in patients with aspirin-sensitive urticaria. Aspirin 88-95 mitochondrially encoded cytochrome c oxidase II Homo sapiens 37-42 15163023-1 2004 Cyclooxygenase (COX)-2, the recently described inducible form ofcyclooxygenase, has been shown to be responsible for the inflammatory and tumorigenic effects of prostaglandins; hence the development and expanding clinical use of COX-2 selective inhibitors termed super aspirins. Aspirin 269-277 mitochondrially encoded cytochrome c oxidase II Homo sapiens 229-234 14742690-0 2004 Aspirin-mediated COX-2 transcript stabilization via sustained p38 activation in human intestinal myofibroblasts. Aspirin 0-7 mitochondrially encoded cytochrome c oxidase II Homo sapiens 17-22 14975457-2 2004 Aspirin and older agents in this class are nonselective inhibitors of both COX-1 and COX-2. Aspirin 0-7 mitochondrially encoded cytochrome c oxidase II Homo sapiens 85-90 14725573-4 2004 In 2003, the results of studies suggest, and guidelines recommend, the careful selection of anti-inflammatory drugs - NSAIDs or selective COX-2 inhibitors (coxibs) based upon patients gastrointestinal history and use of aspirin therapy. Aspirin 220-227 mitochondrially encoded cytochrome c oxidase II Homo sapiens 138-143 14742690-2 2004 In human intestinal myofibroblasts, aspirin, at therapeutic doses, had the unexpected effect of inducing prolonged COX-2 expression. Aspirin 36-43 mitochondrially encoded cytochrome c oxidase II Homo sapiens 115-120 14742690-3 2004 This induction was especially pronounced when cells were treated with interleukin-1alpha (IL-1) plus aspirin for 24 h. Sodium salicylate, a poor COX inhibitor, likewise enhanced IL-1-mediated COX-2 gene expression whereas 5-aminosalicylic acid (5-ASA) or indomethacin had no effect. Aspirin 101-108 mitochondrially encoded cytochrome c oxidase II Homo sapiens 192-197 14742690-4 2004 The COX-2 transcriptional rate, measured by nuclear runoff analysis and heterogeneous nuclear RNA reverse transcription-polymerase chain reaction, was only modestly elevated by aspirin treatment. Aspirin 177-184 mitochondrially encoded cytochrome c oxidase II Homo sapiens 4-9 14742690-5 2004 In contrast, aspirin treatment dramatically stabilized the COX-2 message. Aspirin 13-20 mitochondrially encoded cytochrome c oxidase II Homo sapiens 59-64 14742690-6 2004 The COX-2 mRNA half-life in IL-1 treated cells was 1 h and was increased in excess of 5 h in IL-1 + aspirin-treated cells. Aspirin 100-107 mitochondrially encoded cytochrome c oxidase II Homo sapiens 4-9 14742690-8 2004 Inhibition of p38 activity negated aspirin-mediated COX-2 mRNA stabilization and the resultant increase in COX-2 mRNA and protein levels. Aspirin 35-42 mitochondrially encoded cytochrome c oxidase II Homo sapiens 52-57 14742690-10 2004 We conclude that aspirin enhances COX-2 expression via sustained activation of p38, which results in prolonged stabilization of the COX-2 message and a slightly elevated transcription rate. Aspirin 17-24 mitochondrially encoded cytochrome c oxidase II Homo sapiens 34-39 14742690-10 2004 We conclude that aspirin enhances COX-2 expression via sustained activation of p38, which results in prolonged stabilization of the COX-2 message and a slightly elevated transcription rate. Aspirin 17-24 mitochondrially encoded cytochrome c oxidase II Homo sapiens 132-137 15061569-14 2004 ASA inhibits COX-1 and converts COX-2 into an ASA-triggered lipid mediator-generating system that produces an array of novel endogenous local autacoids from dietary omega-3 PUFA. Aspirin 0-3 mitochondrially encoded cytochrome c oxidase II Homo sapiens 32-37 14965321-7 2004 During the past forty years systematic advances in our understanding of the structure, regulation and function of COX isoenzymes have enabled the design and synthesis of COX-2 selective inhibitors as agents intended to lessen the gastrointestinal irritation of aspirin and non-selective NSAIDs. Aspirin 261-268 mitochondrially encoded cytochrome c oxidase II Homo sapiens 170-175 15383758-14 2004 The use of NSAIDS and aspirin, most likely via inhibition of COX-2 and other inflammatory pathways, is associated with a reduction of adenocarcinoma rates. Aspirin 22-29 mitochondrially encoded cytochrome c oxidase II Homo sapiens 61-66 14584890-2 2003 Significantly higher BMD was found in users of relative COX-2 selective NSAIDs with aspirin (COX-2/ASA) compared with nonusers. Aspirin 84-91 mitochondrially encoded cytochrome c oxidase II Homo sapiens 56-61 14623265-6 2003 The guanylyl-cyclase inhibitor ODQ partially reversed the suppression of COX-2 activity by NO-aspirin, demonstrating a role of cGMP increase. Aspirin 94-101 mitochondrially encoded cytochrome c oxidase II Homo sapiens 73-78 14763357-11 2003 The benefit related to the IN SUMMARY: Cox-2 specific antagonists seems dramatically reduced by the concomitant aspirin intake. Aspirin 112-119 mitochondrially encoded cytochrome c oxidase II Homo sapiens 39-44 14640056-2 2003 The mechanisms by which acetylsalicylic acid and other NSAIDs, including COX-2 inhibitors, exert this effect include: inhibition of COX-2, induction of apoptosis and induction of the P21 protein that controls the development of crypt cells. Aspirin 24-44 mitochondrially encoded cytochrome c oxidase II Homo sapiens 73-78 14640056-2 2003 The mechanisms by which acetylsalicylic acid and other NSAIDs, including COX-2 inhibitors, exert this effect include: inhibition of COX-2, induction of apoptosis and induction of the P21 protein that controls the development of crypt cells. Aspirin 24-44 mitochondrially encoded cytochrome c oxidase II Homo sapiens 132-137 15482000-9 2004 The COX-2 hypothesis proposes that aspirin causes a structural change in COX-2 that results in the generation of products of the lipoxygenase pathway. Aspirin 35-42 mitochondrially encoded cytochrome c oxidase II Homo sapiens 4-9 15482000-9 2004 The COX-2 hypothesis proposes that aspirin causes a structural change in COX-2 that results in the generation of products of the lipoxygenase pathway. Aspirin 35-42 mitochondrially encoded cytochrome c oxidase II Homo sapiens 73-78 14633677-5 2003 Interestingly, NO-ASA induced COX-2 expression, although it had no effect on COX-1. Aspirin 18-21 mitochondrially encoded cytochrome c oxidase II Homo sapiens 30-35 14584890-2 2003 Significantly higher BMD was found in users of relative COX-2 selective NSAIDs with aspirin (COX-2/ASA) compared with nonusers. Aspirin 84-91 mitochondrially encoded cytochrome c oxidase II Homo sapiens 93-98 14584890-2 2003 Significantly higher BMD was found in users of relative COX-2 selective NSAIDs with aspirin (COX-2/ASA) compared with nonusers. Aspirin 99-102 mitochondrially encoded cytochrome c oxidase II Homo sapiens 56-61 14584890-12 2003 RESULTS: After adjustment for possible confounders, current use of relative COX-2 selective NSAIDs with aspirin was associated with higher BMD at the whole body (4.2%, 1.2-7.3 CI) and total hip (4.6%, 0.5-8.8 CI) by DXA and at both trabecular (34.1%, 15.4-52.7 CI) and cortical spine (12.8%, 2.3-23.3 CI) by quantitative computed tomography. Aspirin 104-111 mitochondrially encoded cytochrome c oxidase II Homo sapiens 76-81 14584890-13 2003 CONCLUSIONS: Our data suggest that the combination of relative COX-2 selective NSAIDs and aspirin is associated with higher BMD at multiple skeletal sites in men and women. Aspirin 90-97 mitochondrially encoded cytochrome c oxidase II Homo sapiens 63-68 12960371-1 2003 In addition to inhibiting cyclooxygenase (COX)-1-derived prostanoid biosynthesis, aspirin acetylates COX-2, enabling the conversion of arachidonic acid to 15(R)-epi lipoxin A4, or aspirin-triggered lipoxin (ATL). Aspirin 82-89 mitochondrially encoded cytochrome c oxidase II Homo sapiens 101-106 12960371-1 2003 In addition to inhibiting cyclooxygenase (COX)-1-derived prostanoid biosynthesis, aspirin acetylates COX-2, enabling the conversion of arachidonic acid to 15(R)-epi lipoxin A4, or aspirin-triggered lipoxin (ATL). Aspirin 180-187 mitochondrially encoded cytochrome c oxidase II Homo sapiens 101-106 15199473-3 2003 Aspirin is less effective in inhibiting COX-2 activity, whereas celecoxib and rofecoxib selectively inhibit COX-2 activity as they contain a side chain to anchor to the side pocket of COX-2 substrate channel. Aspirin 0-7 mitochondrially encoded cytochrome c oxidase II Homo sapiens 40-45 12769697-8 2003 The first of these relates to the unique mode of action of aspirin, which acetylates the COX-2 enzyme and generates the cancer-suppressing 15R-hydroxyeicosatetraenoic acid at the site of a potential tumour. Aspirin 59-66 mitochondrially encoded cytochrome c oxidase II Homo sapiens 89-94 12910692-7 2003 Immunohistochemistry and immunoblotting indicated that aspirin effectively decreased COX-2 and c-fos expression in SGC-7901 cell. Aspirin 55-62 mitochondrially encoded cytochrome c oxidase II Homo sapiens 85-90 12910692-10 2003 The anti-neoplastic effect aspirin produces may involve the inhibition of COX-2 expression and AP-1 activity. Aspirin 27-34 mitochondrially encoded cytochrome c oxidase II Homo sapiens 74-79 12904261-6 2003 COX-2 inhibition may decrease endothelial inflammation reducing monocytes infiltration improving vascular cells function, plaque stability and probably resulting in a decrease of coronary atherothrombotic events.Trials including large numbers of patients in prospective double-blind randomized studies worthwhile to confirm the efficacy of NSAID, mainly, COX-2 inhibitors, together with aspirin in the prevention of coronary events in patients with acute coronary disease. Aspirin 387-394 mitochondrially encoded cytochrome c oxidase II Homo sapiens 0-5 14592547-0 2003 Control of COX-2 and iNOS gene expressions by aspirin and salicylate. Aspirin 46-53 mitochondrially encoded cytochrome c oxidase II Homo sapiens 11-16 14592549-2 2003 An incomplete suppression of platelet thromboxane (TX) A2 biosynthesis has been assumed to participate in the phenomenon of aspirin resistance, as a consequence of the following possible mechanisms: (i) COX-2 expression in newly formed platelets; (ii) pharmacodynamic interactions between aspirin and coadministered nonsteroidal antiinflammatory drugs (e.g. ibuprofen); (iii) expression of variant isoforms of COX-1 with reduced sensitivity to irreversible inactivation at Ser529. Aspirin 124-131 mitochondrially encoded cytochrome c oxidase II Homo sapiens 203-208 14592549-4 2003 Thus, in a subset of patients with unstable angina treated with low-dose aspirin, to almost completely block platelet COX-1 activity, enhanced TXA2 biosynthesis in vivo has been demonstrated, presumably through an increased generation of COX-2-dependent PGH2 in plaque monocytes/macrophages or activated vascular cells. Aspirin 73-80 mitochondrially encoded cytochrome c oxidase II Homo sapiens 238-243 12870263-2 2003 The biological effects induced by aspirin and indomethacin on T98G cells, in which the expression of cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2) were confirmed by RT-PCR and immunostaining, were investigated by studying cell proliferation and apoptosis assays. Aspirin 34-41 mitochondrially encoded cytochrome c oxidase II Homo sapiens 148-153 14594936-4 2003 Previous clinical trials have shown the effectiveness of the following: polyprenoic acid (acyclic retinoid) for hepatocellular carcinoma; tamoxifen for breast cancer; retinoic acids for head and neck tumor; and aspirin, a COX-2 inhibitor, for colorectal cancer. Aspirin 211-218 mitochondrially encoded cytochrome c oxidase II Homo sapiens 222-227 12874188-8 2003 The inducible isoform of cyclooxygenase in platelets, COX-2, has been suggested to confer aspirin resistance. Aspirin 90-97 mitochondrially encoded cytochrome c oxidase II Homo sapiens 54-59 12890715-1 2003 (1) Unlike other nonsteroidal anti-inflammatory drugs that inhibit formation of cyclooxygenase (COX)-dependent eicosanoids, acetylation of COX-2 by aspirin switches eicosanoid biosynthesis from prostaglandin E(2) (PGE(2)) to 15-epi-lipoxin A(4) (15-epi-LXA(4) or aspirin-triggered lipoxin, ATL). Aspirin 148-155 mitochondrially encoded cytochrome c oxidase II Homo sapiens 139-144 12890715-1 2003 (1) Unlike other nonsteroidal anti-inflammatory drugs that inhibit formation of cyclooxygenase (COX)-dependent eicosanoids, acetylation of COX-2 by aspirin switches eicosanoid biosynthesis from prostaglandin E(2) (PGE(2)) to 15-epi-lipoxin A(4) (15-epi-LXA(4) or aspirin-triggered lipoxin, ATL). Aspirin 263-270 mitochondrially encoded cytochrome c oxidase II Homo sapiens 139-144 12890715-3 2003 (2) In the present study, we have examined the role of acetylated COX-2 and 5-LOX in modulating antiadhesive effects of aspirin on adhesion of PMN to endotoxin (LPS)-primed human umbilical endothelial cells (HUVEC). Aspirin 120-127 mitochondrially encoded cytochrome c oxidase II Homo sapiens 66-77 12890715-5 2003 Treating HUVEC with selective COX-2 inhibitors, celecoxib and rofecoxib, caused an approximately 70% reversion of antiadhesive effect of aspirin. Aspirin 137-144 mitochondrially encoded cytochrome c oxidase II Homo sapiens 30-35 12622739-0 2003 Transcriptional regulation of COX-2: a key mechanism in the pathogenesis of nasal polyposis in aspirin-sensitive asthmatics? Aspirin 95-102 mitochondrially encoded cytochrome c oxidase II Homo sapiens 30-35 12767724-3 2003 Selective COX-2 inhibitors are effective anti-inflammatory agents with lower gastrointestinal toxicity than aspirin. Aspirin 108-115 mitochondrially encoded cytochrome c oxidase II Homo sapiens 10-15 12618325-6 2003 The possibility of COX-2 as a candidate player in cancer development and progression evolved from the epidemiological studies which suggest that regular use of aspirin or other non-steroidal anti-inflammatory drugs could significantly decrease the risk of developing cancers in experimental animals and in humans. Aspirin 160-167 mitochondrially encoded cytochrome c oxidase II Homo sapiens 19-24 15199473-4 2003 Aspirin and salicylate at therapeutic concentrations inhibit COX-2 protein expression through interference with binding of CCAAT/enhancer binding protein beta (C/EBPbeta) to its cognate site on COX-2 promoter/enhancer. Aspirin 0-7 mitochondrially encoded cytochrome c oxidase II Homo sapiens 61-66 15199473-4 2003 Aspirin and salicylate at therapeutic concentrations inhibit COX-2 protein expression through interference with binding of CCAAT/enhancer binding protein beta (C/EBPbeta) to its cognate site on COX-2 promoter/enhancer. Aspirin 0-7 mitochondrially encoded cytochrome c oxidase II Homo sapiens 194-199 12527817-3 2003 One of these, triacetylsalicylhydroxamic acid (TriAcSHA) was more effective than aspirin and O-acetylsalicylhydroxamic acid in inactivating both COX-1 and COX-2. Aspirin 81-88 mitochondrially encoded cytochrome c oxidase II Homo sapiens 155-160 12391014-1 2002 Aspirin (ASA) is unique among current therapies because it acetylates cyclooxygenase (COX)-2 enabling the biosynthesis of R-containing precursors of endogenous antiinflammatory mediators. Aspirin 0-7 mitochondrially encoded cytochrome c oxidase II Homo sapiens 70-92 12456256-0 2002 Aspirin use may change cost-effectiveness of COX-2 inhibitors. Aspirin 0-7 mitochondrially encoded cytochrome c oxidase II Homo sapiens 45-50 12512737-4 2002 Similarly, the use of nonaspirin nonsteroidal antiinflammatory drugs (NSAIDs), including cyclooxygenase (COX)-2 inhibitors, has also been shown to increase the risk of GI effects, and the concomitant use of aspirin and nonaspirin NSAIDs can significantly increase the risk of GI ulceration and bleeding. Aspirin 25-32 mitochondrially encoded cytochrome c oxidase II Homo sapiens 89-111 12423318-0 2002 COX-2-independent antiproliferative action of acetylsalicylic acid in human colon cancer cells. Aspirin 46-66 mitochondrially encoded cytochrome c oxidase II Homo sapiens 0-5 12716445-3 2003 Large outcome studies have shown that patients with OA and RA not taking low-dose aspirin have fewer symptomatic and complicated upper GI events when treated with COX-2 selective inhibitors than with nonselective NSAIDs. Aspirin 82-89 mitochondrially encoded cytochrome c oxidase II Homo sapiens 163-168 14758788-7 2003 Because coxibs do not inhibit platelet aggregation, if prophylaxis against thromboembolic disease is required in patients being treated with a selective COX-2 inhibitor, low-dose aspirin should be used in conjunction with the coxib. Aspirin 179-186 mitochondrially encoded cytochrome c oxidase II Homo sapiens 153-158 12391014-1 2002 Aspirin (ASA) is unique among current therapies because it acetylates cyclooxygenase (COX)-2 enabling the biosynthesis of R-containing precursors of endogenous antiinflammatory mediators. Aspirin 9-12 mitochondrially encoded cytochrome c oxidase II Homo sapiens 70-92 12391014-4 2002 Human COX-2 converted DHA to 13-hydroxy-DHA that switched with ASA to 17R-HDHA that also proved a major route in hypoxic endothelial cells. Aspirin 63-66 mitochondrially encoded cytochrome c oxidase II Homo sapiens 6-11 12391014-5 2002 Human neutrophils transformed COX-2-ASA-derived 17R-hydroxy-DHA into two sets of novel di- and trihydroxy products; one initiated via oxygenation at carbon 7 and the other at carbon 4. Aspirin 36-39 mitochondrially encoded cytochrome c oxidase II Homo sapiens 30-35 11742186-6 2001 Co-administration of the COX-2 selective NSAID, celecoxib, and low-dose aspirin, is associated with the same risk for upper gastrointestinal ulcer complications alone and combined with symptomatic ulcers, as the non-selective NSAIDs, ibuprofen and diclofenac. Aspirin 72-79 mitochondrially encoded cytochrome c oxidase II Homo sapiens 25-30 12395741-4 2002 THE INFLUENCE OF A CO-PRESCRIPTION OF ASPIRIN: Patients for whom low-dose aspirin is indicated to offset known thrombotic risk must continue this therapy if a COX-2 selective inhibitor is introduced. Aspirin 38-45 mitochondrially encoded cytochrome c oxidase II Homo sapiens 159-164 12395741-4 2002 THE INFLUENCE OF A CO-PRESCRIPTION OF ASPIRIN: Patients for whom low-dose aspirin is indicated to offset known thrombotic risk must continue this therapy if a COX-2 selective inhibitor is introduced. Aspirin 74-81 mitochondrially encoded cytochrome c oxidase II Homo sapiens 159-164 24728118-5 2002 Particularly in patients treated with low-dose of aspirin for cardiovascular prophylaxis, the COX-2 inhibitors seem to have no obvious advantages over conventional NSAIDs. Aspirin 50-57 mitochondrially encoded cytochrome c oxidase II Homo sapiens 94-99 11994707-3 2002 OBJECTIVE: The aim of these studies was to investigate Cox-1 and Cox-2 regulation in NPs of aspirin-tolerant human patients compared with that seen in nasal mucosa (NM). Aspirin 92-99 mitochondrially encoded cytochrome c oxidase II Homo sapiens 65-70 11994707-8 2002 CONCLUSION: These data showing an abnormal regulation of Cox-1 and Cox-2 in NPs from aspirin-tolerant patients reinforce the concept that prostanoid metabolism might be important in the pathogenesis of inflammatory nasal diseases and suggest a potential role for this alteration in the formation of NPs. Aspirin 85-92 mitochondrially encoded cytochrome c oxidase II Homo sapiens 67-72 11823092-2 2002 Aspirin, a nonselective COX-1 (cyclo-oxygenase) and COX-2 inhibitor may result in gastric toxicity. Aspirin 0-7 mitochondrially encoded cytochrome c oxidase II Homo sapiens 52-57 12086293-4 2002 The gastrointestinal toxicity of nonselective NSAIDs and aspirin derives from the inhibition of the cyclooxygenase (COX) enzyme, COX-1, which synthesizes gastroprotective prostaglandins, while the anti-inflammatory and pain-relieving effects are largely derived from inhibition of COX-2-derived prostaglandins. Aspirin 57-64 mitochondrially encoded cytochrome c oxidase II Homo sapiens 281-286 11945152-9 2002 However it is premature to say that the benefit of Cox-2 inhibitors is lost in patients taking aspirin. Aspirin 95-102 mitochondrially encoded cytochrome c oxidase II Homo sapiens 51-56 11717412-8 2001 These results show that a low affinity for Cox-1 and a high degree of Cox-2 selectivity confers a low potential to block aspirin inhibition of platelet Cox-1, consistent with the results of clinical studies. Aspirin 121-128 mitochondrially encoded cytochrome c oxidase II Homo sapiens 70-75 14561202-11 2002 New highly specific COX-2 inhibitors appear to be a safe alternative for patients with aspirin-induced asthma. Aspirin 87-94 mitochondrially encoded cytochrome c oxidase II Homo sapiens 20-25 11251623-0 2001 Safety of a specific COX-2 inhibitor in aspirin-induced asthma. Aspirin 40-47 mitochondrially encoded cytochrome c oxidase II Homo sapiens 21-26 11695246-8 2001 Further studies are needed to determine whether COX-2 selective inhibitors are safer than nonselective NSAIDs when used in patients receiving low-dose aspirin. Aspirin 151-158 mitochondrially encoded cytochrome c oxidase II Homo sapiens 48-53 11566042-9 2001 Use of aspirin in the class study has shown that the benefits of COX-2 inhibitors may be reduced by aspirin use. Aspirin 7-14 mitochondrially encoded cytochrome c oxidase II Homo sapiens 65-70 11566042-9 2001 Use of aspirin in the class study has shown that the benefits of COX-2 inhibitors may be reduced by aspirin use. Aspirin 100-107 mitochondrially encoded cytochrome c oxidase II Homo sapiens 65-70 11577463-0 2001 [Cyclooxygenase (COX)-2 selective inhibitors: aspirin, a dual COX-1/COX-2 inhibitor, to COX-2 selective inhibitors]. Aspirin 46-53 mitochondrially encoded cytochrome c oxidase II Homo sapiens 68-73 11577463-2 2001 During the century after that, aspirin has been found to show its anti-inflammatory, analgesic and anti-pyretic activities by reducing prostaglandins biosynthesis through inhibition of cyclooxygenase (COX); and then COX was found to be constituted of two isoforms, constitutive COX-1 and inducible COX-2. Aspirin 31-38 mitochondrially encoded cytochrome c oxidase II Homo sapiens 298-303 11577463-3 2001 Currently, novel NSAIDs, acting through selective inhibition of COX-2, that have efficacy as excellent as aspirin with significantly lower incidence of gastrointestinal adverse effects are available in America and some other countries, but not in Japan. Aspirin 106-113 mitochondrially encoded cytochrome c oxidase II Homo sapiens 64-69 11266647-3 2001 Indeed, development of the new "super aspirins," such as Celebrex and Vioxx, that selectively inhibit the inducible COX-2, expressed in areas of inflammation, is a direct outgrowth of this concept. Aspirin 38-46 mitochondrially encoded cytochrome c oxidase II Homo sapiens 116-121 11173047-2 2001 Aspirin, conventional nonsteroidal anti-inflammatory drugs (NSAIDs), and COX-2-specific inhibitors exhibit different patterns of inhibition of COX-1-mediated thromboxane biosynthesis and COX-2-mediated prostacyclin biosynthesis. Aspirin 0-7 mitochondrially encoded cytochrome c oxidase II Homo sapiens 187-192 11251623-1 2001 In a subset of patients with asthma, aspirin and several other non-steroidal anti-inflammatory drugs (NSAID) that inhibit simultaneously cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2) precipitate dangerous asthmatic attacks. Aspirin 37-44 mitochondrially encoded cytochrome c oxidase II Homo sapiens 184-189 11235048-3 2001 Current prescribing information warns to avoid using COX-2 inhibitors in aspirin-sensitive asthma patients. Aspirin 73-80 mitochondrially encoded cytochrome c oxidase II Homo sapiens 53-58 11235048-4 2001 New evidence suggests that aspirin sensitivity may be linked to the COX-1 pathway, and COX-2 inhibitors, as a result of their selectivity, may be beneficial in patients with aspirin-induced asthma. Aspirin 174-181 mitochondrially encoded cytochrome c oxidase II Homo sapiens 87-92 11552047-8 2001 Aspirin is a more potent inhibitor of Cox-1 than of Cox-2, unlike other non-steroidal anti-inflammatory drugs (NSAIDs), which have limited selectivity. Aspirin 0-7 mitochondrially encoded cytochrome c oxidase II Homo sapiens 52-57 11437671-4 2001 The development of novel "super aspirins" with high selectivity towards the inhibition of COX-2 showed that this hypothesis was well-founded and that high levels of these drugs could be tolerated without these serious adverse effects. Aspirin 32-40 mitochondrially encoded cytochrome c oxidase II Homo sapiens 90-95 11078056-5 2000 In contrast, aspirin-like nonselective NSAIDs such as sulindac and indomethacin inhibit not only the enzymatic action of the highly inducible, proinflammatory COX-2 but the constitutively expressed, cytoprotective COX-1 as well. Aspirin 13-20 mitochondrially encoded cytochrome c oxidase II Homo sapiens 159-164 17018963-12 2000 All aspirinlike drugs have until quite recently been mixed blockers of cyclooxigenases (COX 1 and COX 2) with aspirin itself being the most outstanding COX 1 blocker. Aspirin 4-11 mitochondrially encoded cytochrome c oxidase II Homo sapiens 98-103 12120179-1 2001 One hundred years after the introduction of aspirin, greater understanding of the mechanism of action of NSAIDs has led to the development of selective COX-2 inhibitors. Aspirin 44-51 mitochondrially encoded cytochrome c oxidase II Homo sapiens 152-157 11211927-7 2000 Using the mean of the results for PGE2 and TXB2 inhibition, the COX-1/COX-2 ratios of the IC50 values for aspirin and NS-398 are < 0.1 and > 130, respectively. Aspirin 106-113 mitochondrially encoded cytochrome c oxidase II Homo sapiens 70-75 11211927-9 2000 Dose responses to aspirin and NS-398 which are COX- and COX-2 selective inhibitors respectively, confirmed the utility of this system. Aspirin 18-25 mitochondrially encoded cytochrome c oxidase II Homo sapiens 56-61 10992560-0 2000 The importance of COX-2 inhibition for aspirin induced asthma. Aspirin 39-46 mitochondrially encoded cytochrome c oxidase II Homo sapiens 18-23 10639016-2 1999 Since aspirin is a weak inhibitor of the inducible isoform of prostaglandin H synthase (COX-2), it was suggested that COX-2 may play a role in aspirin resistance. Aspirin 6-13 mitochondrially encoded cytochrome c oxidase II Homo sapiens 88-93 10942685-1 2000 OBJECTIVES: the preventive effect of acetylsalicylic acid in cardiovascular disease may be due to inhibition of platelet aggregation mediated by COX-1, but may in addition be due to anti-inflammatory effects by inhibition of COX-2. Aspirin 37-57 mitochondrially encoded cytochrome c oxidase II Homo sapiens 225-230 10977131-10 2000 After incubation with LPS plus acetylsalicylic acid, positive staining was observed for both COX-1-ir and COX-2-ir. Aspirin 31-51 mitochondrially encoded cytochrome c oxidase II Homo sapiens 106-111 11055820-10 2000 However, the well known contraindications for NSAIDs, such as late pregnancy, aspirin-induced asthma, congestive heart failure and renal dysfunction, will so far apply also to the COX-2 inhibitors. Aspirin 78-85 mitochondrially encoded cytochrome c oxidase II Homo sapiens 180-185 10868686-6 2000 Bile acids could induce COX-2 expression in six of eight cell lines tested, which was correlated with prostaglandin E2 production, and aspirin could inhibit COX-2 enzymatic activity even after bile acid stimulation but was unable to change the COX-2 protein level in these cell lines. Aspirin 135-142 mitochondrially encoded cytochrome c oxidase II Homo sapiens 157-162 10868686-6 2000 Bile acids could induce COX-2 expression in six of eight cell lines tested, which was correlated with prostaglandin E2 production, and aspirin could inhibit COX-2 enzymatic activity even after bile acid stimulation but was unable to change the COX-2 protein level in these cell lines. Aspirin 135-142 mitochondrially encoded cytochrome c oxidase II Homo sapiens 157-162 10671506-6 2000 To understand the changes that lead to 15R-HETE synthesis in aspirin-treated COX-2, we employed pro-R- and pro-S-labeled [13-(3)H]arachidonic acids to investigate the selectivity of the initial hydrogen abstraction. Aspirin 61-68 mitochondrially encoded cytochrome c oxidase II Homo sapiens 77-82 10671506-7 2000 Remarkably, aspirin-treated COX-2 formed 15R-HETE with removal of the pro-S hydrogen at C-13 (3-9% retention of pro-S tritium label), the same stereoselectivity as in the formation of prostaglandins by native cyclooxygenase. Aspirin 12-19 mitochondrially encoded cytochrome c oxidase II Homo sapiens 28-33 10639016-2 1999 Since aspirin is a weak inhibitor of the inducible isoform of prostaglandin H synthase (COX-2), it was suggested that COX-2 may play a role in aspirin resistance. Aspirin 6-13 mitochondrially encoded cytochrome c oxidase II Homo sapiens 118-123 10639016-2 1999 Since aspirin is a weak inhibitor of the inducible isoform of prostaglandin H synthase (COX-2), it was suggested that COX-2 may play a role in aspirin resistance. Aspirin 143-150 mitochondrially encoded cytochrome c oxidase II Homo sapiens 88-93 10639016-2 1999 Since aspirin is a weak inhibitor of the inducible isoform of prostaglandin H synthase (COX-2), it was suggested that COX-2 may play a role in aspirin resistance. Aspirin 143-150 mitochondrially encoded cytochrome c oxidase II Homo sapiens 118-123 10639016-3 1999 However the cellular source(s) of COX-2 possibly responsible for aspirin resistance remains unknown. Aspirin 65-72 mitochondrially encoded cytochrome c oxidase II Homo sapiens 34-39 10639016-9 1999 Our results argue against the involvement of COX-2 in TX biosynthesis by activated platelets and consequently dispute platelet COX-2 expression as an important mechanism of aspirin resistance. Aspirin 173-180 mitochondrially encoded cytochrome c oxidase II Homo sapiens 127-132 8718891-10 1996 ASA-acetylated apo-hCox-2 shows the same fluorescence-quenching behavior in the presence of most of the above inhibitors. Aspirin 0-3 mitochondrially encoded cytochrome c oxidase II Homo sapiens 19-25 10390414-4 1999 We hypothesize that an abnormal regulation of COX-2 will predispose patients with asthma to develop aspirin-intolerant asthma/rhinitis (AIAR). Aspirin 100-107 mitochondrially encoded cytochrome c oxidase II Homo sapiens 46-51 10220459-2 1999 In this report, the effects of aspirin and sodium salicylate on COX-2 expressions in human umbilical vein endothelial cells and foreskin fibroblasts were evaluated. Aspirin 31-38 mitochondrially encoded cytochrome c oxidase II Homo sapiens 64-69 12973429-10 1999 This difference is therapeutically significant and selective inhibitors of COX-2 exhibit antiinflammatory potency without the gastric and renal toxicities of the aspirin-like drugs. Aspirin 162-169 mitochondrially encoded cytochrome c oxidase II Homo sapiens 75-80 9831328-9 1998 In addition, the well-known protective action of aspirin on colon cancer may be through an action on COX-2, which is expressed in this disease. Aspirin 49-56 mitochondrially encoded cytochrome c oxidase II Homo sapiens 101-106 9831331-5 1998 The lowest COX-2 selectivities, which means the highest COX-1 selectivities, were observed in indomethacin, aspirin, and oxaprozin. Aspirin 108-115 mitochondrially encoded cytochrome c oxidase II Homo sapiens 11-16 9515564-1 1998 Aspirin and conventional nonsteroidal anti-inflammatory drugs are nonselective inhibitors of cyclooxygenase-1 (COX-1) and COX-2 enzymes. Aspirin 0-7 mitochondrially encoded cytochrome c oxidase II Homo sapiens 122-127 9475035-14 1997 Older nonsteroidal antiinflammatory drugs like aspirin and indomethacin are non selective inhibitors of COX activity and therefore, in addition to inhibiting COX-2 activity, inhibit the formation of eicosanoids by COX-1. Aspirin 47-54 mitochondrially encoded cytochrome c oxidase II Homo sapiens 158-163 9372101-2 1996 Recent studies suggest that aspirin"s anti-inflammatory effects are mediated via inhibition of an inducible isoform of cyclooxygenase in inflammatory cells (COX-2) and through blockade of the nuclear transcription factor, NF-kappa B. Aspirin 28-35 mitochondrially encoded cytochrome c oxidase II Homo sapiens 157-162 10381057-16 1999 Aspirin and piroxicam were about 8 times more active against COX-1 than COX-2, indomethacin was 7 times more active, and diclofenac was an equipotent inhibitor of COX-1 and COX-2. Aspirin 0-7 mitochondrially encoded cytochrome c oxidase II Homo sapiens 72-77 10381057-16 1999 Aspirin and piroxicam were about 8 times more active against COX-1 than COX-2, indomethacin was 7 times more active, and diclofenac was an equipotent inhibitor of COX-1 and COX-2. Aspirin 0-7 mitochondrially encoded cytochrome c oxidase II Homo sapiens 173-178 9263351-3 1997 Aspirin is an approximately 150- to 200-fold more potent inhibitor of the (constitutive) isoform of the platelet enzyme (COX-1) than the (inducible) isoform (COX-2) which is expressed by cytokines, inflammatory stimuli, and some growth factors. Aspirin 0-7 mitochondrially encoded cytochrome c oxidase II Homo sapiens 158-163 9263351-4 1997 This explains the different dosage requirements of aspirin as an antithrombotic (COX-1) and an anti-inflammatory drug (COX-2), respectively. Aspirin 51-58 mitochondrially encoded cytochrome c oxidase II Homo sapiens 119-124 35441670-4 2022 Our aims were to compare the effects of low-dose (COX-1 inhibition) and high-dose (dual COX-1 and COX-2 inhibition) aspirin on blood pressure, vascular function, oxidative stress, ET-1 and prostanoid levels and kidney damage during angiogenesis inhibitor therapy in rodents. Aspirin 116-123 mitochondrially encoded cytochrome c oxidase II Homo sapiens 98-103 34775204-10 2021 Many of the synthesized agents show enhanced COX-1/2 properties than aspirin with better selectivity index towards COX-2 relative to COX-1. Aspirin 69-76 mitochondrially encoded cytochrome c oxidase II Homo sapiens 115-120 34822026-4 2022 Furthermore, we describe other potential benefits related to aspirin-triggered lipoxins and resolvins while illustrating how NSAIDs interfere with COX-1, COX-2, SARS-CoV-2/ SARS-CoV-2 ORF protein-dependent activation of caspases and their subsequent mitochondrial dysfunction, endoplasmic reticulum stress, apoptosis and necroptosis which were associated with COVID-19 complications. Aspirin 61-68 mitochondrially encoded cytochrome c oxidase II Homo sapiens 154-159 34700376-7 2021 In HCAE cells, overexpressed genes included EFNA1 and LIF, two genes commonly upregulated in colorectal cancer and associated with poor patient outcomes, and PTGS2 (COX2), a gene associated with the protective effect of aspirin in the colorectal cancer setting. Aspirin 220-227 mitochondrially encoded cytochrome c oxidase II Homo sapiens 165-169 34201817-6 2021 The inhibition of COX-2 enzyme activity, but not protein expression was observed for ASA and one Salix extract. Aspirin 85-88 mitochondrially encoded cytochrome c oxidase II Homo sapiens 18-23 34893997-1 2022 Derivatives of the cytotoxic cyclooxygenase (COX) inhibitor ((prop-2-ynyl)-2-acetoxybenzoate)dicobalthexacarbonyl (Co-ASS) with a methyl group in the 3, 4, 5, or 6 position of the acetylsalicylic acid (ASS) scaffold were synthesized with the aim to achieve enhanced selectivity for COX-2. Aspirin 180-200 mitochondrially encoded cytochrome c oxidase II Homo sapiens 282-287 34428217-6 2021 In contrast, indomethacin did not exhibit this capacity, whereas cyclooxygenase (COX)-2 selective NSAID, celecoxib, induced a similar pattern like Acetylsalicylic acid, suggesting a possible relevance of COX-2. Aspirin 147-167 mitochondrially encoded cytochrome c oxidase II Homo sapiens 65-87 34428217-6 2021 In contrast, indomethacin did not exhibit this capacity, whereas cyclooxygenase (COX)-2 selective NSAID, celecoxib, induced a similar pattern like Acetylsalicylic acid, suggesting a possible relevance of COX-2. Aspirin 147-167 mitochondrially encoded cytochrome c oxidase II Homo sapiens 204-209 34376069-4 2022 Co-therapy with aspirin reduces the GI benefits of COX-2 selective agents, whereas ibuprofen and naproxen may neglect the antiplatelet effect of aspirin. Aspirin 16-23 mitochondrially encoded cytochrome c oxidase II Homo sapiens 51-56 34122428-4 2021 Celecoxib, a selective COX-2 inhibitor, and aspirin, a non-selective COX-1 and COX-2 inhibitor, are being used as anti-inflammatory, analgesic and anti-pyretic drugs. Aspirin 44-51 mitochondrially encoded cytochrome c oxidase II Homo sapiens 79-84 35067692-4 2022 It has been shown that the biosynthesis of SPMs called eicosapentaenoic acid (EPA)-derived E-series resolvins is initiated by aspirin-acetylated COX-2 from EPA, leading to 18-hydroperoxy-eicosapentaenoic acid (18-HpEPE). Aspirin 126-133 mitochondrially encoded cytochrome c oxidase II Homo sapiens 145-150 35373259-3 2022 Compared with colorectal cancer, the role of aspirin in gastric cancer prevention is less well described, however it stands to reason that aspirin and/or other nonsteroidal anti-inflammatory drugs may inhibit gastric cancer progression through the inhibition of COX-2. Aspirin 139-146 mitochondrially encoded cytochrome c oxidase II Homo sapiens 262-267 35067692-7 2022 By contrast, in the aspirin-acetylated COX-2/EPA complex, the H16proS-abstraction energy barriers are somewhat lower than the H13proS energy barriers and much smaller than the H16-transfer barriers in the wild type COX-2/EPA system. Aspirin 20-27 mitochondrially encoded cytochrome c oxidase II Homo sapiens 39-44 35067692-7 2022 By contrast, in the aspirin-acetylated COX-2/EPA complex, the H16proS-abstraction energy barriers are somewhat lower than the H13proS energy barriers and much smaller than the H16-transfer barriers in the wild type COX-2/EPA system. Aspirin 20-27 mitochondrially encoded cytochrome c oxidase II Homo sapiens 215-220 35067692-9 2022 In the following step of the catalytic mechanism, the calculated O2 addition to C18 is preferred versus the addition to C14 which also agrees with 18R-HEPE and 18S-HEPE being the main products from EPA in aspirin-acetylated COX-2. Aspirin 205-212 mitochondrially encoded cytochrome c oxidase II Homo sapiens 224-229 34029712-3 2021 Symptoms due to increased baseline and/or episodic release of PGD2 can be prevented with aspirin, an inhibitor of cyclooxygenase (COX)1 and COX2. Aspirin 89-96 mitochondrially encoded cytochrome c oxidase II Homo sapiens 140-144 35000048-0 2022 COX-1, COX-2 and CYP2C19 variations may be related to cardiovascular events due to acetylsalicylic acid resistance. Aspirin 83-103 mitochondrially encoded cytochrome c oxidase II Homo sapiens 7-12 34983353-2 2022 By affecting the cyclooxygenase 1 and 2 (COX-1 and COX-2) enzymes and actin filaments, acetylsalicylic acid (Aspirin) has been shown to reduce the risk of breast cancer and prevent cell migration in both laboratory and clinical studies. Aspirin 87-107 mitochondrially encoded cytochrome c oxidase II Homo sapiens 51-56 34983353-2 2022 By affecting the cyclooxygenase 1 and 2 (COX-1 and COX-2) enzymes and actin filaments, acetylsalicylic acid (Aspirin) has been shown to reduce the risk of breast cancer and prevent cell migration in both laboratory and clinical studies. Aspirin 109-116 mitochondrially encoded cytochrome c oxidase II Homo sapiens 51-56 32535107-1 2020 The most recognized mechanism of aspirin(acetylsalicylic acid, ASA) action, at therapeutic dosing, is the inhibition of prostanoid biosynthesis through the acetylation of cyclooxygenase(COX)-isozymes (COX-1 at serine-529 and COX-2 at serine-516). Aspirin 33-40 mitochondrially encoded cytochrome c oxidase II Homo sapiens 225-230 33975019-3 2021 The treatment with ASA caused an increase in the gene expression of COX2 and ABCB1 in both MDR cell lines, and a decrease in the expression of ALOX5 in the FEPS cells. Aspirin 19-22 mitochondrially encoded cytochrome c oxidase II Homo sapiens 68-72 32997790-5 2021 Although the exact mode of action remains unclear, multiple downstream effects of aspirin may interfere with cholangiocarcinogenesis, tumour growth, and metastasis-including inhibiting the COX-2 pathway, preventing platelet aggregation, and modulating certain proteins and signalling. Aspirin 82-89 mitochondrially encoded cytochrome c oxidase II Homo sapiens 189-194 33430037-10 2021 PTGS2/COX2 expression trended lower in aspirin users, but not with tumor response. Aspirin 39-46 mitochondrially encoded cytochrome c oxidase II Homo sapiens 6-10 31420920-0 2020 Aspirin for the prevention and treatment of pre-eclampsia: A matter of COX-1 and/or COX-2 inhibition? Aspirin 0-7 mitochondrially encoded cytochrome c oxidase II Homo sapiens 84-89 32535107-5 2020 Hu-COX-2 exposed in vitro to an excess of ASA was acetylated by approximately 40-50% associated with the inhibition of COX-2 activity by 80-90%. Aspirin 42-45 mitochondrially encoded cytochrome c oxidase II Homo sapiens 3-8 32535107-5 2020 Hu-COX-2 exposed in vitro to an excess of ASA was acetylated by approximately 40-50% associated with the inhibition of COX-2 activity by 80-90%. Aspirin 42-45 mitochondrially encoded cytochrome c oxidase II Homo sapiens 119-124 32535107-6 2020 In the three cell-types expressing COX-2, the extent of COX-2 acetylation and reduction of prostaglandin (PG)E2 biosynthesis by ASA was concentration-dependent with comparable EC50 values(in the low muM range). Aspirin 128-131 mitochondrially encoded cytochrome c oxidase II Homo sapiens 35-40 32535107-6 2020 In the three cell-types expressing COX-2, the extent of COX-2 acetylation and reduction of prostaglandin (PG)E2 biosynthesis by ASA was concentration-dependent with comparable EC50 values(in the low muM range). Aspirin 128-131 mitochondrially encoded cytochrome c oxidase II Homo sapiens 56-61 32535107-8 2020 In conclusion, we have developed a proteomic assay to evaluate the extent of acetylation of COX-2 at serine-516 by aspirin; its use in clinical studies will allow clarifying the mechanism of action of aspirin as anticancer agent. Aspirin 115-122 mitochondrially encoded cytochrome c oxidase II Homo sapiens 92-97 32535107-8 2020 In conclusion, we have developed a proteomic assay to evaluate the extent of acetylation of COX-2 at serine-516 by aspirin; its use in clinical studies will allow clarifying the mechanism of action of aspirin as anticancer agent. Aspirin 201-208 mitochondrially encoded cytochrome c oxidase II Homo sapiens 92-97 33618245-4 2021 OBSERVATIONS: This paper reviews randomized controlled trials that showed that celecoxib, a selective COX-2 inhibitor, or low-dose aspirin, which inhibits COX-1 and inhibits/acetylates COX-2, reduced bipolar symptoms in patients on mood stabilizers. Aspirin 131-138 mitochondrially encoded cytochrome c oxidase II Homo sapiens 185-190 33618245-6 2021 CONCLUSIONS: This clinical evidence is consistent with the hypothesis that low-dose chronic aspirin and celecoxib, which can inhibit COX-2 and enter brain, can be repurposed in bipolar disorder to enhance mood stabilizer effects on arachidonic acid metabolism and neurotransmission. Aspirin 92-99 mitochondrially encoded cytochrome c oxidase II Homo sapiens 133-138 33293599-6 2020 COX-2 induction was prevented by different antiplatelet agents, i.e., Aspirin, the TP antagonist SQ29,548, or Revacept (a dimeric soluble GPVI-Fc fusion protein). Aspirin 70-77 mitochondrially encoded cytochrome c oxidase II Homo sapiens 0-5 32535107-1 2020 The most recognized mechanism of aspirin(acetylsalicylic acid, ASA) action, at therapeutic dosing, is the inhibition of prostanoid biosynthesis through the acetylation of cyclooxygenase(COX)-isozymes (COX-1 at serine-529 and COX-2 at serine-516). Aspirin 41-61 mitochondrially encoded cytochrome c oxidase II Homo sapiens 225-230 32535107-1 2020 The most recognized mechanism of aspirin(acetylsalicylic acid, ASA) action, at therapeutic dosing, is the inhibition of prostanoid biosynthesis through the acetylation of cyclooxygenase(COX)-isozymes (COX-1 at serine-529 and COX-2 at serine-516). Aspirin 63-66 mitochondrially encoded cytochrome c oxidase II Homo sapiens 225-230 32535107-2 2020 Whether aspirin, also when given at the low-doses recommended for cardiovascular prevention, reduces the risk of colorectal cancer by affecting COX-2 activity in colorectal adenomatous lesions is still debated. Aspirin 8-15 mitochondrially encoded cytochrome c oxidase II Homo sapiens 144-149 32535107-3 2020 We aimed to develop a direct biomarker of aspirin action on COX-2 by assessing the extent of acetylation of COX-2 at serine-516 using the AQUA strategy, enabling absolute protein quantitation by liquid chromatography-mass spectrometry. Aspirin 42-49 mitochondrially encoded cytochrome c oxidase II Homo sapiens 60-65 32535107-3 2020 We aimed to develop a direct biomarker of aspirin action on COX-2 by assessing the extent of acetylation of COX-2 at serine-516 using the AQUA strategy, enabling absolute protein quantitation by liquid chromatography-mass spectrometry. Aspirin 42-49 mitochondrially encoded cytochrome c oxidase II Homo sapiens 108-113 32646396-13 2020 In addition, the survival benefit of postdiagnosis aspirin use appeared to be confined to patients with mutated PIK3CA tumors [HR = 0.78, 95%CI(0.50, 0.99)] and was positive for PTGS2 (COX-2) expression [HR = 0.75, 95%CI(0.43, 1.30)]. Aspirin 51-58 mitochondrially encoded cytochrome c oxidase II Homo sapiens 185-190 32646396-14 2020 CONCLUSIONS: These findings provide further indications that postdiagnosis aspirin use improves overall survival and cancer-specific survival in colorectal cancer, especially for patients who are positive for PTGS2 (COX-2) expression and PIK3CA-mutated tumors. Aspirin 75-82 mitochondrially encoded cytochrome c oxidase II Homo sapiens 216-221 31005060-9 2019 CONCLUSIONS: Aspirin 15 cH acts through the inhibition of the COX-2 pathway producing a clear pro-thrombotic effect. Aspirin 14-21 mitochondrially encoded cytochrome c oxidase II Homo sapiens 63-68 31905343-0 2020 Aspirin enhances the sensitivity of colon cancer cells to cisplatin by abrogating the binding of NF-kappaB to the COX-2 promoter. Aspirin 0-7 mitochondrially encoded cytochrome c oxidase II Homo sapiens 114-119 31905343-7 2020 In addition, we demonstrated that the enhanced effect of aspirin on the cisplatin-induced inhibition of tumor cell growth was also mediated through the suppression of the binding activity of NF-kappaB to the COX-2 promoter. Aspirin 57-64 mitochondrially encoded cytochrome c oxidase II Homo sapiens 208-213 31905343-8 2020 The combination of aspirin and cisplatin effectively attenuated the translocation of NF-kappaB p65/p50 from the cytoplasm to the nucleus, and abrogated the binding of NF-kappaB p65/p50 to the COX-2 promoter, thereby down-regulating COX-2 expression and PGE2 synthesis. Aspirin 19-26 mitochondrially encoded cytochrome c oxidase II Homo sapiens 192-197 31905343-8 2020 The combination of aspirin and cisplatin effectively attenuated the translocation of NF-kappaB p65/p50 from the cytoplasm to the nucleus, and abrogated the binding of NF-kappaB p65/p50 to the COX-2 promoter, thereby down-regulating COX-2 expression and PGE2 synthesis. Aspirin 19-26 mitochondrially encoded cytochrome c oxidase II Homo sapiens 232-237 31586705-6 2019 The results of this study indicate that the new derivatives of OAO and particularly their conjugates with ASP, downregulate the expression of COX-2 in HepG2 cells by modulating the NF-kappaB signaling pathway and suggest their potential application in the prevention of liver inflammation and cancer. Aspirin 106-109 mitochondrially encoded cytochrome c oxidase II Homo sapiens 142-147 32218705-6 2020 Aspirin inhibited COX-2 and iNOS without changes in COX-1 expression, increasing anti-oxidant protein (Cu/Zn-SOD and Mn-SOD) expression in presence or absence of Abeta1-42. Aspirin 0-7 mitochondrially encoded cytochrome c oxidase II Homo sapiens 18-23 32181121-0 2020 Structural modification of aspirin to design a new potential cyclooxygenase (COX-2) inhibitors. Aspirin 27-34 mitochondrially encoded cytochrome c oxidase II Homo sapiens 77-82