PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 34920958-2 2022 Cyclooxygenase-2(COX-2) and its metabolite prostaglandins are known to promote the inflammatory resolution of ARDS. Prostaglandins 43-57 cytochrome c oxidase II, mitochondrial Rattus norvegicus 17-22 34776980-11 2021 In conclusion, Guizhi Fuling Capsules can effectively relieve primary dysmenorrhea, and this effect may be attributed to the regulation effects of Guizhi Fuling Capsules on endogenous metabolism, such as inhibiting arachidonic acid converted to prostaglandins through downregulate the expression of COX-2, which plays an anti-inflammatory effect. Prostaglandins 245-259 cytochrome c oxidase II, mitochondrial Rattus norvegicus 299-304 34836047-10 2021 Copper NPs in a standard daily dose had more significant effects on the mechanism(s) responsible for the utilization of reactive oxygen species in the blood plasma with the participation of prostanoids derived from COX-2 in the vascular relaxation. Prostaglandins 190-201 cytochrome c oxidase II, mitochondrial Rattus norvegicus 215-220 25780555-9 2014 VP-induced vasoconstriction in younger MA F utilized both COX-1 and COX-2 derived constrictor prostanoids. Prostaglandins 94-105 cytochrome c oxidase II, mitochondrial Rattus norvegicus 68-73 31378306-4 2019 Cox2 is one of two Cox isoenzymes that is responsible for the formation of prostanoids from arachidonic acid. Prostaglandins 75-86 cytochrome c oxidase II, mitochondrial Rattus norvegicus 0-4 30442654-14 2019 This latter action may be developed by COX-2-liberated prostaglandins. Prostaglandins 55-69 cytochrome c oxidase II, mitochondrial Rattus norvegicus 39-44 30618728-10 2018 Crocetin inhibited the COX-2 catalyzed prostaglandin (PGE2) and inducible nitric oxide synthase catalyzed NO production on RAW 264.7. Prostaglandins 39-52 cytochrome c oxidase II, mitochondrial Rattus norvegicus 23-28 30144443-7 2018 This association between the COX-2 and PGE2 levels suggests that the enzyme activity is the likely factor that determines the synthesis and levels of the prostaglandin in the culture media of the granulosa-derived cells. Prostaglandins 154-167 cytochrome c oxidase II, mitochondrial Rattus norvegicus 29-34 29602230-7 2018 Further studies on the mechanism underlying this phenomenon showed a correlation between decreased expression of phosphorylated cytosolic phospholipase A2 (p-cPLA2) and increased mRNA and protein expression of COX2, potentially leading to a deeper understanding of altered AA and prostaglandin levels in ovarian tissues of PCOS rats. Prostaglandins 280-293 cytochrome c oxidase II, mitochondrial Rattus norvegicus 210-214 27834752-11 2016 CONCLUSIONS: These results show that the juvenile rat brains mostly respond to ischemia by a COX-2-dependent prostaglandins production and suggest that the transcriptional responses observed under 7-NI facilitate and reorient COX-2-dependent prostaglandins production. Prostaglandins 109-123 cytochrome c oxidase II, mitochondrial Rattus norvegicus 93-98 27834752-11 2016 CONCLUSIONS: These results show that the juvenile rat brains mostly respond to ischemia by a COX-2-dependent prostaglandins production and suggest that the transcriptional responses observed under 7-NI facilitate and reorient COX-2-dependent prostaglandins production. Prostaglandins 109-123 cytochrome c oxidase II, mitochondrial Rattus norvegicus 226-231 27834752-11 2016 CONCLUSIONS: These results show that the juvenile rat brains mostly respond to ischemia by a COX-2-dependent prostaglandins production and suggest that the transcriptional responses observed under 7-NI facilitate and reorient COX-2-dependent prostaglandins production. Prostaglandins 242-256 cytochrome c oxidase II, mitochondrial Rattus norvegicus 93-98 27834752-11 2016 CONCLUSIONS: These results show that the juvenile rat brains mostly respond to ischemia by a COX-2-dependent prostaglandins production and suggest that the transcriptional responses observed under 7-NI facilitate and reorient COX-2-dependent prostaglandins production. Prostaglandins 242-256 cytochrome c oxidase II, mitochondrial Rattus norvegicus 226-231 26934930-7 2016 In the femoral arteries of SHR, the production of prostanoids [6-keto prostaglandin (PG)F1alpha (a metabolite of prostacyclin (PGI2), PGE2, and PGF2alpha] and COX-2 protein were increased compared with that in WKY rats. Prostaglandins 50-61 cytochrome c oxidase II, mitochondrial Rattus norvegicus 159-164 26774808-8 2015 A partial prostaglandin synthesis block caused by COX-2 inhibitor (meloxicam) caused no significant changes of evaluated HRV parameters compared to the control. Prostaglandins 10-23 cytochrome c oxidase II, mitochondrial Rattus norvegicus 50-55 25216050-10 2014 Prostanoids derived from both isoforms helped maintain vasoconstriction in LZR while in OZR only COX-2 was active. Prostaglandins 0-11 cytochrome c oxidase II, mitochondrial Rattus norvegicus 97-102 31841390-0 2020 COX-2 derived prostaglandins as mediators of the deleterious effects of nicotine in chronic kidney disease. Prostaglandins 14-28 cytochrome c oxidase II, mitochondrial Rattus norvegicus 0-5 31841390-9 2020 Treatment with the COX-2 inhibitor NS-398 resulted in complete inhibition of all prostaglandins studied and ameliorated renal injury and proteinuria in 5/6Nx rats on nicotine but not in 5/6 Nx rats on tap water. Prostaglandins 81-95 cytochrome c oxidase II, mitochondrial Rattus norvegicus 19-24 31378306-14 2019 Cox2-derived prostaglandins might play a role in brain-renin angiotensin system associated hypertension, and astrocytes could be significant players. Prostaglandins 13-27 cytochrome c oxidase II, mitochondrial Rattus norvegicus 0-4 31247902-2 2019 Cyclooxygenase (COX), a rate-limiting enzyme responsible for the biosynthesis of prostaglandins (PGs), exists in two isoforms: COX-1, the constitutive form, and COX-2, mainly the inducible form. Prostaglandins 81-95 cytochrome c oxidase II, mitochondrial Rattus norvegicus 161-166 31247902-2 2019 Cyclooxygenase (COX), a rate-limiting enzyme responsible for the biosynthesis of prostaglandins (PGs), exists in two isoforms: COX-1, the constitutive form, and COX-2, mainly the inducible form. Prostaglandins 97-100 cytochrome c oxidase II, mitochondrial Rattus norvegicus 161-166 31247902-3 2019 COX-2 is the key enzyme in eicosanoid metabolism that converts eicosanoids into a number of PGs, including PGD2, PGE2, PGF2alpha, and prostacyclin (PGI2), all of which exert diverse hormone-like effects via autocrine or paracrine mechanisms. Prostaglandins 92-95 cytochrome c oxidase II, mitochondrial Rattus norvegicus 0-5 29755544-2 2018 Nonsteroidal anti-inflammatory drugs (NSAIDs) act mainly via inhibition of prostaglandins synthesis by inhibition of cyclooxygenase (COX) isoenzymes (COX-1 and COX-2). Prostaglandins 75-89 cytochrome c oxidase II, mitochondrial Rattus norvegicus 160-165 28706454-2 2017 Prostaglandins (produced by COX-1 and COX-2) play an important role in the contractile response to phenylephrine in the abdominal aorta of young rats. Prostaglandins 0-14 cytochrome c oxidase II, mitochondrial Rattus norvegicus 38-43 24854565-3 2014 Cyclooxygenase (COX)-2 is the inducible isoform of an intracellular enzyme that converts arachidonic acid into prostaglandins. Prostaglandins 111-125 cytochrome c oxidase II, mitochondrial Rattus norvegicus 0-22 24532118-4 2014 In inflammatory tissues, COX-2 is greatly expressed producing proinflammatory prostaglandins (PGs). Prostaglandins 78-92 cytochrome c oxidase II, mitochondrial Rattus norvegicus 25-30 24532118-4 2014 In inflammatory tissues, COX-2 is greatly expressed producing proinflammatory prostaglandins (PGs). Prostaglandins 94-97 cytochrome c oxidase II, mitochondrial Rattus norvegicus 25-30 23254481-2 2013 Cyclooxygenase (COX)-2 is a protein involved in the biosynthesis of inflammatory prostaglandins. Prostaglandins 93-107 cytochrome c oxidase II, mitochondrial Rattus norvegicus 0-22 24012611-11 2013 The results also suggest that basal release of COX-2-derived vasoconstrictor prostanoids is involved in renal vascular hypersensitivity in SHR. Prostaglandins 77-88 cytochrome c oxidase II, mitochondrial Rattus norvegicus 47-52 23624225-0 2013 COX2-derived primary and cyclopentenone prostaglandins are increased after asphyxial cardiac arrest. Prostaglandins 40-54 cytochrome c oxidase II, mitochondrial Rattus norvegicus 0-4 24012611-4 2013 The kidneys were isolated to measure perfusion pressure and COX-1- or COX-2-derived prostanoids in response to alpha1-AR activation. Prostaglandins 84-95 cytochrome c oxidase II, mitochondrial Rattus norvegicus 70-75 22436072-0 2012 Effect of age and COX-2-derived prostanoids on the progression of adult vascular dysfunction in the offspring of diabetic rats. Prostaglandins 32-43 cytochrome c oxidase II, mitochondrial Rattus norvegicus 18-23 22311599-5 2012 COX2-mediated prostaglandin production and postsynaptic activation of a Src family tyrosine kinase were required. Prostaglandins 14-27 cytochrome c oxidase II, mitochondrial Rattus norvegicus 0-4 21940154-5 2012 Dietary CLA resulted in ~32%-53% lower levels of prostanoids produced by total COX and COX2 activities in normal and diseased kidneys and partially mitigated alterations in COX2 protein levels associated with disease. Prostaglandins 49-60 cytochrome c oxidase II, mitochondrial Rattus norvegicus 87-91 21940154-10 2012 The effects of CLA feeding on COX2 protein levels and activity indicate that the beneficial effect of dietary CLA in this renal disorder is mediated in part via effects on COX2-derived prostanoids. Prostaglandins 185-196 cytochrome c oxidase II, mitochondrial Rattus norvegicus 30-34 21940154-10 2012 The effects of CLA feeding on COX2 protein levels and activity indicate that the beneficial effect of dietary CLA in this renal disorder is mediated in part via effects on COX2-derived prostanoids. Prostaglandins 185-196 cytochrome c oxidase II, mitochondrial Rattus norvegicus 172-176 22411738-4 2012 Elevated levels of COX-2 were seen in the DMBA group, the enzyme responsible for prostaglandin synthesis during inflammation and cancer, whilst the expression of the constitutive isoform, COX-1, was equally expressed in all the groups. Prostaglandins 81-94 cytochrome c oxidase II, mitochondrial Rattus norvegicus 19-24 23090753-1 2013 Prostaglandins (PGs), whose synthesis is catalyzed by the rate-limiting enzyme cyclooxygenase (COX) including COX-1 and COX-2, are among the important mediators involved in the regulation of gonadotropin-releasing hormone (GnRH) secretion. Prostaglandins 0-14 cytochrome c oxidase II, mitochondrial Rattus norvegicus 120-125 23090753-1 2013 Prostaglandins (PGs), whose synthesis is catalyzed by the rate-limiting enzyme cyclooxygenase (COX) including COX-1 and COX-2, are among the important mediators involved in the regulation of gonadotropin-releasing hormone (GnRH) secretion. Prostaglandins 16-19 cytochrome c oxidase II, mitochondrial Rattus norvegicus 120-125 21939736-2 2011 The inducible cyclooxygenase COX-2, which along with COX-1 catalyzes the first committed step in prostaglandin (PG) synthesis, elicits significant brain injury in models of cerebral ischemia; however its downstream PG receptor pathways trigger both toxic and paradoxically protective effects. Prostaglandins 97-110 cytochrome c oxidase II, mitochondrial Rattus norvegicus 29-34 22249337-4 2012 TNF-alpha up-regulation activates nuclear factor kappaB, which further up-regulates cyclooxygenase (COX)-2 leading to altered prostaglandin profile. Prostaglandins 126-139 cytochrome c oxidase II, mitochondrial Rattus norvegicus 84-106 22249337-5 2012 Inhibition of TNF-alpha and COX-2 provides beneficial effect on diabetic neuropathy by decreasing the oxidative stress level and by preventing neuronal hypersensitivity due to an increased prostaglandin level. Prostaglandins 189-202 cytochrome c oxidase II, mitochondrial Rattus norvegicus 28-33 22220238-1 2011 BACKGROUND: The analgesic mechanisms of cyclooxygenase (COX)-2 inhibitors have been explained mainly on the basis of the inhibition of prostaglandin biosynthesis. Prostaglandins 135-148 cytochrome c oxidase II, mitochondrial Rattus norvegicus 40-62 23209788-12 2012 As increased contractile response in resistance vessels may contribute to hypertension, our results suggest a role for these COX-2-derived prostanoids in elevating vascular resistance and blood pressure in offspring of diabetic rats. Prostaglandins 139-150 cytochrome c oxidase II, mitochondrial Rattus norvegicus 125-130 21939736-2 2011 The inducible cyclooxygenase COX-2, which along with COX-1 catalyzes the first committed step in prostaglandin (PG) synthesis, elicits significant brain injury in models of cerebral ischemia; however its downstream PG receptor pathways trigger both toxic and paradoxically protective effects. Prostaglandins 112-114 cytochrome c oxidase II, mitochondrial Rattus norvegicus 29-34 21745460-2 2011 Traditional NSAIDs inhibit both cyclooxygenases-1 and 2 (COX-1, 2), which act as key enzymes catalyzing the same reaction in the production of prostaglandins (PGs), while the second class of NSAIDs selectively inhibit COX-2. Prostaglandins 143-157 cytochrome c oxidase II, mitochondrial Rattus norvegicus 218-223 21745460-2 2011 Traditional NSAIDs inhibit both cyclooxygenases-1 and 2 (COX-1, 2), which act as key enzymes catalyzing the same reaction in the production of prostaglandins (PGs), while the second class of NSAIDs selectively inhibit COX-2. Prostaglandins 159-162 cytochrome c oxidase II, mitochondrial Rattus norvegicus 218-223 21272267-12 2011 These data suggest that downregulation of COX-2 is responsible for impaired de novo generation of vasodilatory prostaglandins which may play an important role for the CP induced renal vasoconstriction and development of nephropathy. Prostaglandins 111-125 cytochrome c oxidase II, mitochondrial Rattus norvegicus 42-47 21239635-1 2011 Cyclooxygenase (COX)-2 expression is increased in the kidney of rats made diabetic with streptozotocin and associated with enhanced release of prostaglandins stimulated by arachidonic acid (AA). Prostaglandins 143-157 cytochrome c oxidase II, mitochondrial Rattus norvegicus 0-22 19693696-1 2010 Cyclooxygenase (COX), which have the isoforms of COX-1 and COX-2, is the key enzyme of prostaglandins biosynthesis. Prostaglandins 87-101 cytochrome c oxidase II, mitochondrial Rattus norvegicus 59-64 21273786-12 2011 This vascular dysfunction was related to COX-2-derived prostanoids and oxidative stress, increased pro- inflammatory cytokines and reduced NO bioavailability. Prostaglandins 55-66 cytochrome c oxidase II, mitochondrial Rattus norvegicus 41-46 20147610-0 2010 Urinary tract obstruction induces transient accumulation of COX-2-derived prostanoids in kidney tissue. Prostaglandins 74-85 cytochrome c oxidase II, mitochondrial Rattus norvegicus 60-65 20147610-2 2010 We hypothesized that BUO leads to COX-2-mediated local accumulation of prostanoids in inner medulla (IM) tissue. Prostaglandins 71-82 cytochrome c oxidase II, mitochondrial Rattus norvegicus 34-39 20147610-16 2010 In BUO, therapeutic interventions aimed at the COX-prostanoid pathway should target primarily COX-2. Prostaglandins 51-61 cytochrome c oxidase II, mitochondrial Rattus norvegicus 94-99 20036891-6 2010 These findings suggest that prostanoids, which are produced by constitutively active COX-2, influence the contractile response of the abdominal aorta and that the production of arachidonic acid relies on phospholipase C and diacylglycerol lipase. Prostaglandins 28-39 cytochrome c oxidase II, mitochondrial Rattus norvegicus 85-90 20043943-2 2010 COX-1 and COX-2 converts arachidonic acid into prostaglandins. Prostaglandins 47-61 cytochrome c oxidase II, mitochondrial Rattus norvegicus 10-15 20082610-10 2010 CONCLUSIONS AND IMPLICATIONS: Vasoactive prostanoids were formed via constitutively active COX-1 and COX-2 pathways in normal rat penile arteries. Prostaglandins 41-52 cytochrome c oxidase II, mitochondrial Rattus norvegicus 101-106 19789943-1 2010 BACKGROUND: Nonsteroidal anti-inflammatory drugs act by inhibiting the rate-limiting enzymes cyclooxygenase-1 (Cox-1) and cyclooxygenase-2 (Cox-2), which are important in prostanoid formation. Prostaglandins 171-181 cytochrome c oxidase II, mitochondrial Rattus norvegicus 140-145 20228412-0 2010 The role of cyclooxygenase (COX)-2 derived prostanoids on vasoconstrictor responses to phenylephrine is increased by exposure to low mercury concentration. Prostaglandins 43-54 cytochrome c oxidase II, mitochondrial Rattus norvegicus 12-34 18344592-2 2008 Cyclooxygenase (COX)-2 has recently emerged as a key regulator of PG synthesis. Prostaglandins 66-68 cytochrome c oxidase II, mitochondrial Rattus norvegicus 0-22 19615686-12 2010 CONCLUSIONS: In hyperhomocysteinemia increases in flow/shear stress increases the production of COX-2-derived TxA(2), and reactive oxygen species--that overcome the dilator effects of NO and prostaglandins--eliciting constrictions in skeletal muscle venules; changes which can increase vascular resistance and favor thrombus formation in the venular circulation. Prostaglandins 191-205 cytochrome c oxidase II, mitochondrial Rattus norvegicus 96-101 19567483-14 2009 CONCLUSION: Despite the prevalence of vasoconstrictor prostanoids derived from COX-2 in aortas from ovariectomized rats, the ACh-induced relaxation is maintained, probably as consequence of the positive regulation that prostanoids exert on eNOS activity. Prostaglandins 54-65 cytochrome c oxidase II, mitochondrial Rattus norvegicus 79-84 19418724-15 2009 These results suggest that NO produced via iNOS and PGs produced by COX-1/COX-2, have an important role in the pathogenesis of cystitis induced by ACR. Prostaglandins 52-55 cytochrome c oxidase II, mitochondrial Rattus norvegicus 74-79 18946499-9 2009 Our findings show that COX-2 derived prostanoids downregulate OATs during lipopolysaccharide-induced acute renal injury. Prostaglandins 37-48 cytochrome c oxidase II, mitochondrial Rattus norvegicus 23-28 18310519-12 2008 These data reveal that estrogen enhances constrictor prostanoid function in female rat aorta by upregulating the expression of COX-2 and TxS in both Endo and VSM and by upregulating the expression of TP in VSM. Prostaglandins 53-63 cytochrome c oxidase II, mitochondrial Rattus norvegicus 127-132 17929312-6 2008 These results indicate that up-regulated neuronal COX-2 would be involved in aberrant brain excitation-induced NREM sleep via production of PGs. Prostaglandins 140-143 cytochrome c oxidase II, mitochondrial Rattus norvegicus 50-55 21303331-1 2010 Nonsteroidal anti-inflammatory drugs (NSAIDs) have been shown to be effective antineoplastic agents that block prostaglandin formation by inhibiting the enzyme cyclooxygenase (COX), which exists in two isoforms, COX-1 and COX-2. Prostaglandins 111-124 cytochrome c oxidase II, mitochondrial Rattus norvegicus 222-227 19041231-1 2009 Selective COX-2 inhibitor, celecoxib, delays the healing of gastric ulcers by inhibiting prostaglandins synthesis. Prostaglandins 89-103 cytochrome c oxidase II, mitochondrial Rattus norvegicus 10-15 17622965-3 2007 COX-2-generated prostaglandins are important regulators for a range of activities under physiologic conditions. Prostaglandins 16-30 cytochrome c oxidase II, mitochondrial Rattus norvegicus 0-5 17559081-2 2008 Because COX-2 is the rate-limiting step in the production of PGs, mechanisms that regulate COX-2 expression control PG production in the cell. Prostaglandins 61-64 cytochrome c oxidase II, mitochondrial Rattus norvegicus 8-13 17559081-2 2008 Because COX-2 is the rate-limiting step in the production of PGs, mechanisms that regulate COX-2 expression control PG production in the cell. Prostaglandins 61-64 cytochrome c oxidase II, mitochondrial Rattus norvegicus 91-96 17559081-2 2008 Because COX-2 is the rate-limiting step in the production of PGs, mechanisms that regulate COX-2 expression control PG production in the cell. Prostaglandins 61-63 cytochrome c oxidase II, mitochondrial Rattus norvegicus 8-13 17559081-2 2008 Because COX-2 is the rate-limiting step in the production of PGs, mechanisms that regulate COX-2 expression control PG production in the cell. Prostaglandins 61-63 cytochrome c oxidase II, mitochondrial Rattus norvegicus 91-96 18236017-2 2007 It selectively inhibits cyclooxygenase II (COX-2) enzyme which is responsible for the production of proinflammatory prostanoids. Prostaglandins 116-127 cytochrome c oxidase II, mitochondrial Rattus norvegicus 43-48 18028778-2 2007 COX-2 is the inducible enzyme in the COX family, together with the prostanoids forms the COX-2/prostanoid pathway. Prostaglandins 67-78 cytochrome c oxidase II, mitochondrial Rattus norvegicus 0-5 18028778-2 2007 COX-2 is the inducible enzyme in the COX family, together with the prostanoids forms the COX-2/prostanoid pathway. Prostaglandins 67-78 cytochrome c oxidase II, mitochondrial Rattus norvegicus 89-94 18028778-2 2007 COX-2 is the inducible enzyme in the COX family, together with the prostanoids forms the COX-2/prostanoid pathway. Prostaglandins 67-77 cytochrome c oxidase II, mitochondrial Rattus norvegicus 0-5 18028778-2 2007 COX-2 is the inducible enzyme in the COX family, together with the prostanoids forms the COX-2/prostanoid pathway. Prostaglandins 67-77 cytochrome c oxidase II, mitochondrial Rattus norvegicus 89-94 18028778-3 2007 Research showed that the COX-2/prostanoid pathway is activated in hepatic diseases and liver stress reaction, such as fibrogenesis, portal hypertension, carcinogenesis, and ischemic/reperfusion injury. Prostaglandins 31-41 cytochrome c oxidase II, mitochondrial Rattus norvegicus 25-30 18028778-5 2007 This study was to investigate the role of the COX-2/prostanoid pathway in liver stress response in rat acute colitis visceral pain liver stress model. Prostaglandins 52-62 cytochrome c oxidase II, mitochondrial Rattus norvegicus 46-51 17429720-9 2007 These results suggest that endogenous prostaglandins (PGs) afford protection against colonic ulceration, yet the COX isozyme responsible for the production of PGs differs depending on the stage of ulceration; COX-1 in the early stage and COX-2 in the late stage. Prostaglandins 159-162 cytochrome c oxidase II, mitochondrial Rattus norvegicus 238-243 18006440-15 2008 Despite the predominance of vasoconstrictor prostanoids derived from COX-2 in aortas from orchidectomized rats, the ACh-induced relaxation remains increased. Prostaglandins 44-55 cytochrome c oxidase II, mitochondrial Rattus norvegicus 69-74 17622965-4 2007 However, under pathologic conditions, COX-2 activity can produce reactive oxygen species and toxic prostaglandin metabolites that can exacerbate brain injury. Prostaglandins 99-112 cytochrome c oxidase II, mitochondrial Rattus norvegicus 38-43 17258197-10 2007 Moreover, COX-1- and COX-2-derived prostanoids may play differential or sometimes antagonistic roles in the late phase of acute inflammation. Prostaglandins 35-46 cytochrome c oxidase II, mitochondrial Rattus norvegicus 21-26 18028778-17 2007 Liver injury might have occurred through the activation of the COX-2/prostanoid pathway and increased production of PGE2 and TXB2. Prostaglandins 69-79 cytochrome c oxidase II, mitochondrial Rattus norvegicus 63-68 17600550-2 2007 The present study was undertaken to elucidate the effects of parecoxib, a novel cyclo-oxygenase (COX)-2 inhibitor, on spontaneous and prostaglandin-induced contractions of uterine smooth muscle. Prostaglandins 134-147 cytochrome c oxidase II, mitochondrial Rattus norvegicus 80-103 17196338-11 2007 This study shows that both cox isoforms are present in skin and that they have an important role in mediating bradykinin-evoked heat sensitisation of C-MH sensitive fibres through cox-1 and cox-2 dependent prostaglandin synthesis. Prostaglandins 206-219 cytochrome c oxidase II, mitochondrial Rattus norvegicus 190-195 17221297-2 2007 Inhibition of COX-1 up-regulates COX-2 expression, and the prostaglandins (PGs) produced by COX-2 help to maintain the mucosal integrity during inhibition of COX-1. Prostaglandins 59-73 cytochrome c oxidase II, mitochondrial Rattus norvegicus 92-97 17221297-2 2007 Inhibition of COX-1 up-regulates COX-2 expression, and the prostaglandins (PGs) produced by COX-2 help to maintain the mucosal integrity during inhibition of COX-1. Prostaglandins 75-78 cytochrome c oxidase II, mitochondrial Rattus norvegicus 92-97 17244722-11 2007 In conclusion, AT1 receptor activation by Ang II could be involved in the increased participation of COX-2-derived contractile prostanoids in vasoconstriction to phenylephrine with hypertension, probably through COX-2 expression regulation. Prostaglandins 127-138 cytochrome c oxidase II, mitochondrial Rattus norvegicus 101-106 17244722-11 2007 In conclusion, AT1 receptor activation by Ang II could be involved in the increased participation of COX-2-derived contractile prostanoids in vasoconstriction to phenylephrine with hypertension, probably through COX-2 expression regulation. Prostaglandins 127-138 cytochrome c oxidase II, mitochondrial Rattus norvegicus 212-217 17303338-8 2007 The present results suggested that circulating IL-6 could act as a messenger of inflammatory information from peripheral inflammatory sites to the CNS and as the afferent circulating signal to the CNS to produce prostaglandins in the vascular endothelial cells of the CNS through a COX-2 dependent pathway. Prostaglandins 212-226 cytochrome c oxidase II, mitochondrial Rattus norvegicus 282-287 16622181-10 2006 These findings demonstrate that COX-1- and COX-2-derived prostanoids contribute importantly to the development of malignant hypertension in Cyp1a1-Ren2 transgenic rats. Prostaglandins 57-68 cytochrome c oxidase II, mitochondrial Rattus norvegicus 43-48 17201733-2 2007 Cyclo-oxygenase (COX)-2 is involved in constitutive production of prostanoids in the kidney and plays a role in the control of renal function and morphology. Prostaglandins 66-77 cytochrome c oxidase II, mitochondrial Rattus norvegicus 0-23 17084463-2 2007 COX-1 may be the critical isoform required for the production of PG with a homeostatic function, whereas COX-2 may be the main contributor to PG production in inflammation. Prostaglandins 142-144 cytochrome c oxidase II, mitochondrial Rattus norvegicus 105-110 17077517-8 2006 Our results show that prostaglandin production in CECs during stimulated conditions is sensitive to inhibition by 2-methoxycinnamaldehyde and suggest that 2-methoxycinnamaldehyde may reduce COX-2 protein level and activity but not COX-2 mRNA. Prostaglandins 22-35 cytochrome c oxidase II, mitochondrial Rattus norvegicus 190-195 17077517-8 2006 Our results show that prostaglandin production in CECs during stimulated conditions is sensitive to inhibition by 2-methoxycinnamaldehyde and suggest that 2-methoxycinnamaldehyde may reduce COX-2 protein level and activity but not COX-2 mRNA. Prostaglandins 22-35 cytochrome c oxidase II, mitochondrial Rattus norvegicus 231-236 17084463-1 2007 OBJECTIVE: Recently, a selective COX-2 inhibitor was developed and used for reducing the levels of inflammation-inducing prostaglandin (PG) whilst not inhibiting the release of protective PG by COX-1. Prostaglandins 121-134 cytochrome c oxidase II, mitochondrial Rattus norvegicus 33-38 17084463-1 2007 OBJECTIVE: Recently, a selective COX-2 inhibitor was developed and used for reducing the levels of inflammation-inducing prostaglandin (PG) whilst not inhibiting the release of protective PG by COX-1. Prostaglandins 136-138 cytochrome c oxidase II, mitochondrial Rattus norvegicus 33-38 16810556-1 2006 INTRODUCTION: Cox2 inhibitors decrease prostaglandin production and therefore influence bone healing especially in unstable long bone models. Prostaglandins 39-52 cytochrome c oxidase II, mitochondrial Rattus norvegicus 14-18 16569634-7 2006 These results suggest that KA signals directly stimulate the arachidonic acid cascade in the initial phase and that COX-1 and COX-2, both constitutively expressed at low levels, differentially contribute to PG productions. Prostaglandins 207-209 cytochrome c oxidase II, mitochondrial Rattus norvegicus 126-131 16699067-12 2006 In conclusion, endogenous PGs play a role in the healing of intestinal ulcers through EP4 receptors, yet the COX isozyme involved differs depending on the stage of healing; COX-2 in the early stage and COX-1 in the late stage. Prostaglandins 26-29 cytochrome c oxidase II, mitochondrial Rattus norvegicus 173-178 16580130-7 2006 Thus, BK has been shown to induce COX-2 protein by B2 receptor, which may cause prostanoid generation in rat DRG cells, which may play an important role in the pathogenesis of inflammatory pain and hyperalgesia around the primary sensory neurons. Prostaglandins 80-90 cytochrome c oxidase II, mitochondrial Rattus norvegicus 34-39 16464474-6 2006 Although there are many aspects to neuroinflammation, the pathways involving the cyclooxygenase (COX)-2 and subsequent generation of prostaglandin clearly play a role. Prostaglandins 133-146 cytochrome c oxidase II, mitochondrial Rattus norvegicus 81-103 16569634-8 2006 In the late phase, a sustained PG production in hippocampus appears due to the increased COX-2 levels even with a limited arachidonic acid supply. Prostaglandins 31-33 cytochrome c oxidase II, mitochondrial Rattus norvegicus 89-94 17143008-10 2006 These results suggest that endogenous prostaglandins produced by COX-2 play an important role in the healing of DSS-induced colonic lesions. Prostaglandins 38-52 cytochrome c oxidase II, mitochondrial Rattus norvegicus 65-70 16634783-11 2006 CONCLUSIONS: Abdominal surgery increases the synthesis of prostanoids, particularly via the COX-2 isoform. Prostaglandins 58-69 cytochrome c oxidase II, mitochondrial Rattus norvegicus 92-97 16323955-9 2005 The differential expression patterns in the rat placenta, especially of COX-2, imply that there may be gestational changes in the biosynthesis of PGs and other potential bioactive EFA metabolites. Prostaglandins 146-149 cytochrome c oxidase II, mitochondrial Rattus norvegicus 72-77 16008526-5 2005 Whereas the treatment with SC-560 caused a 60-70% inhibition in the total prostanoid content of most tissues examined, a significant decrease (35-50%) in total prostanoid content following selective COX-2 inhibition was solely detected for kidney and brain tissues. Prostaglandins 160-170 cytochrome c oxidase II, mitochondrial Rattus norvegicus 199-204 16008526-7 2005 These results demonstrate that constitutively expressed COX-2 contributes to the production of prostanoids in kidney and brain for each of the PGE2, PGI2 and TXB2 pathways under non-inflammatory conditions. Prostaglandins 95-106 cytochrome c oxidase II, mitochondrial Rattus norvegicus 56-61 16495185-5 2006 CONCLUSION: COX-1 and COX-2 expressions in rat gastric mucosa during the recovery from stress ulcer participate in the recovery of the damaged mucosa possibly by mediating prostaglandin secretion. Prostaglandins 172-185 cytochrome c oxidase II, mitochondrial Rattus norvegicus 22-27 16281994-9 2005 These findings suggest that the COX-2-mediated PG cascade may collaborate with the COX-1 pathway in the regulation of arteriolar myogenic activity in rat gingiva in the case of the supply of a large amount of AA. Prostaglandins 47-49 cytochrome c oxidase II, mitochondrial Rattus norvegicus 32-37 16139265-1 2005 Prostaglandin, a key molecule that stimulates the complex array of ulcer healing mechanism, gets synthesized in the mucosal cells by cyclooxygenase (COX) enzymes: COX-1 and COX-2. Prostaglandins 0-13 cytochrome c oxidase II, mitochondrial Rattus norvegicus 173-178 16011486-3 2005 In the present study, using whole-cell patch clamp recordings of rat neurones in a slice preparation of the PVN, we show that the effects of IL-1beta are abolished in the presence of a cyclooxygenase (COX)-2 inhibitor, NS-398, indicating a dependence on prostaglandin (PG) synthesis and activation. Prostaglandins 254-267 cytochrome c oxidase II, mitochondrial Rattus norvegicus 185-207 16139265-8 2005 Therefore, induction of COX-2 expression leading to higher level of prostaglandin appears to be an important contributing factor in drug mediated ulcer healing apart from the respective mechanisms of different drugs. Prostaglandins 68-81 cytochrome c oxidase II, mitochondrial Rattus norvegicus 24-29 16011486-3 2005 In the present study, using whole-cell patch clamp recordings of rat neurones in a slice preparation of the PVN, we show that the effects of IL-1beta are abolished in the presence of a cyclooxygenase (COX)-2 inhibitor, NS-398, indicating a dependence on prostaglandin (PG) synthesis and activation. Prostaglandins 269-271 cytochrome c oxidase II, mitochondrial Rattus norvegicus 185-207 16053267-6 2005 This paradoxic ulcer and colitis aggravating effect of selective COX-2 inhibitors may be explained by suppression of protective prostaglandins generated as a consequence of COX-2 induction in inflammatory states. Prostaglandins 128-142 cytochrome c oxidase II, mitochondrial Rattus norvegicus 65-70 15927699-5 2005 The effects of IL-1beta on MNC neurons were blocked in the presence of a specific cyclooxygenase (COX)-2 inhibitor, NS-398, indicating a dependence on prostaglandins (PG) in mediating these effects. Prostaglandins 151-165 cytochrome c oxidase II, mitochondrial Rattus norvegicus 82-104 15927699-5 2005 The effects of IL-1beta on MNC neurons were blocked in the presence of a specific cyclooxygenase (COX)-2 inhibitor, NS-398, indicating a dependence on prostaglandins (PG) in mediating these effects. Prostaglandins 167-169 cytochrome c oxidase II, mitochondrial Rattus norvegicus 82-104 16053267-6 2005 This paradoxic ulcer and colitis aggravating effect of selective COX-2 inhibitors may be explained by suppression of protective prostaglandins generated as a consequence of COX-2 induction in inflammatory states. Prostaglandins 128-142 cytochrome c oxidase II, mitochondrial Rattus norvegicus 173-178 15517427-0 2005 Prostaglandin-mediated control of rat brain kynurenic acid synthesis--opposite actions by COX-1 and COX-2 isoforms. Prostaglandins 0-13 cytochrome c oxidase II, mitochondrial Rattus norvegicus 100-105 15862805-8 2005 These results suggest that COX-2-mediated prostaglandins may play an important role in the progression of pathophysiology in this model and that celecoxib may be a useful therapeutic agent for the treatment of rheumatoid arthritis, with greater safety than non-selective COX inhibitors. Prostaglandins 42-56 cytochrome c oxidase II, mitochondrial Rattus norvegicus 27-32 15882258-1 2005 BACKGROUND: Cyclooxygenase (COX) isoforms, COX-1 and COX-2, are involved in production of prostanoids in the kidney. Prostaglandins 90-101 cytochrome c oxidase II, mitochondrial Rattus norvegicus 53-58 15650120-11 2005 NO produced by inducible NOS and prostaglandins synthesized by COX-2 are both involved in the pathogenesis of delayed colonic transit after burn injury. Prostaglandins 33-47 cytochrome c oxidase II, mitochondrial Rattus norvegicus 63-68 15935072-3 2005 Here, we demonstrate that besides COX-2, which is the prominent COX isoform in the brain and particularly in the hippocampus, the constitutive isoform, COX-1 also contributes to prostaglandin (PG) synthesis and oxidative damage following in vivo acute activation of hippocampal NMDA glutamate receptors. Prostaglandins 193-195 cytochrome c oxidase II, mitochondrial Rattus norvegicus 34-39 15650114-8 2005 Because this protein has a completely different amino acid sequence than COX-1 and COX-2 and it does not have cyclooxygenase activity, we suggest a name cyclooxygenase variant protein to distinguish it from the known prostaglandin-synthesizing cyclooxygenase isoforms. Prostaglandins 217-230 cytochrome c oxidase II, mitochondrial Rattus norvegicus 83-88 15618346-9 2005 Our results show that prostaglandin production in CECs during basal and stimulated conditions is very sensitive to inhibition by acetaminophen and suggest that acetaminophen acts against COX-2 and not COX-1 or COX-3. Prostaglandins 22-35 cytochrome c oxidase II, mitochondrial Rattus norvegicus 187-192 16019677-1 2005 PURPOSE: Inflammation, in general, causes the release of a variety of inflammatory mediators that in turn induce cyclooxygenase (COX) 2, nitric oxide synthase (iNOS) and 5-lipoxygense (LP) synthesis, producing large amounts of inflammatory prostaglandins (PG), nitric oxide (NO), and leukotriene (LT) B4. Prostaglandins 240-254 cytochrome c oxidase II, mitochondrial Rattus norvegicus 113-135 16019677-1 2005 PURPOSE: Inflammation, in general, causes the release of a variety of inflammatory mediators that in turn induce cyclooxygenase (COX) 2, nitric oxide synthase (iNOS) and 5-lipoxygense (LP) synthesis, producing large amounts of inflammatory prostaglandins (PG), nitric oxide (NO), and leukotriene (LT) B4. Prostaglandins 256-258 cytochrome c oxidase II, mitochondrial Rattus norvegicus 113-135 15182426-6 2004 Expression of enzymes associated with inflammation, such as inducible nitric oxide synthase (iNOS) and the inducible type of cyclooxygenase (COX), COX-2, is increased in AOM-induced rat colon carcinogenesis, and overproduction of nitric oxide (NO) and prostaglandins is considered to be involved in colon tumor development. Prostaglandins 252-266 cytochrome c oxidase II, mitochondrial Rattus norvegicus 147-152 15371279-11 2004 The in vitro results suggest that the hyperglycemia-induced increase in NO in retinal Muller cells and endothelial cells increases production of cytotoxic prostaglandins via COX-2. Prostaglandins 155-169 cytochrome c oxidase II, mitochondrial Rattus norvegicus 174-179 15149320-10 2004 CONCLUSION: Taken together, our data suggest that CsA acts as an antinatriuretic, likely by the inhibition of COX-2-mediated renal prostanoid formation. Prostaglandins 131-141 cytochrome c oxidase II, mitochondrial Rattus norvegicus 110-115 15149320-11 2004 Since the furosemide-induced stimulation of the renin system is not attenuated by CsA but by COX-2 inhibition, we speculate that extrarenal COX-2-derived prostanoids may be involved in the stimulation of the renin system by CsA and by loop diuretics. Prostaglandins 154-165 cytochrome c oxidase II, mitochondrial Rattus norvegicus 93-98 15149320-11 2004 Since the furosemide-induced stimulation of the renin system is not attenuated by CsA but by COX-2 inhibition, we speculate that extrarenal COX-2-derived prostanoids may be involved in the stimulation of the renin system by CsA and by loop diuretics. Prostaglandins 154-165 cytochrome c oxidase II, mitochondrial Rattus norvegicus 140-145 15067210-6 2004 Aminoguanidine exerts its effect over the PG metabolism by inhibiting COX-II activity and expression. Prostaglandins 42-44 cytochrome c oxidase II, mitochondrial Rattus norvegicus 70-76 15082878-11 2004 These results suggest that endogenous PGs derived from both COX-1 and COX-2 are involved in the mucosal defense of the inflamed stomach, partly by decreasing acid secretion and contribute to maintaining the mucosal integrity under such conditions. Prostaglandins 38-41 cytochrome c oxidase II, mitochondrial Rattus norvegicus 70-75 12900348-1 2003 BACKGROUND: Prostanoid synthesis by the cyclooxygenase (COX)-2 pathway plays an important role in inflammation, and recent studies have shown the presence of COX-2 in the normal rat lung. Prostaglandins 12-22 cytochrome c oxidase II, mitochondrial Rattus norvegicus 158-163 12900348-8 2003 CONCLUSIONS: The results of these experiments suggest that arachidonic acid is converted into vasoactive prostanoids by the COX-2 and COX-1 pathway in the pulmonary and peripheral vascular beds in the rat and that TXA2 is a major prostanoid formed in the normal rat lung. Prostaglandins 105-116 cytochrome c oxidase II, mitochondrial Rattus norvegicus 124-129 12900348-8 2003 CONCLUSIONS: The results of these experiments suggest that arachidonic acid is converted into vasoactive prostanoids by the COX-2 and COX-1 pathway in the pulmonary and peripheral vascular beds in the rat and that TXA2 is a major prostanoid formed in the normal rat lung. Prostaglandins 105-115 cytochrome c oxidase II, mitochondrial Rattus norvegicus 124-129 12714352-12 2003 We hypothesize that, in SHR, lack of downward resetting of the lower limit of autoregulation in response to a prolonged lowering of RPP could be the result of increased COX-2-mediated production of vasoconstrictory prostaglandins. Prostaglandins 215-229 cytochrome c oxidase II, mitochondrial Rattus norvegicus 169-174 12916703-1 2003 The expression of both cyclooxygenase (COX)-1 and COX-2, which are representative enzymes in prostaglandin synthesis, was evaluated in the sciatic nerve of rats with experimental autoimmune neuritis (EAN). Prostaglandins 93-106 cytochrome c oxidase II, mitochondrial Rattus norvegicus 50-55 12798067-13 2003 They further demonstrate that a COX-2 selective NSAID, such as parecoxib (valdecoxib), has only a small effect on delaying fracture healing even at doses that are known to fully inhibit prostaglandin production. Prostaglandins 186-199 cytochrome c oxidase II, mitochondrial Rattus norvegicus 32-37 12832725-2 2003 Also the significance of prostaglandins (PG) generated by constitutive and inducible cyclooxygenase (COX-1 and COX-2) in the stimulation of hypothalamic-pituitary-adrenal (HPA) axis by AVP under basal and crowding stress conditions was investigated. Prostaglandins 25-39 cytochrome c oxidase II, mitochondrial Rattus norvegicus 111-116 12832725-2 2003 Also the significance of prostaglandins (PG) generated by constitutive and inducible cyclooxygenase (COX-1 and COX-2) in the stimulation of hypothalamic-pituitary-adrenal (HPA) axis by AVP under basal and crowding stress conditions was investigated. Prostaglandins 41-43 cytochrome c oxidase II, mitochondrial Rattus norvegicus 111-116 12900348-2 2003 However, the role of COX-2 in the generation of vasoactive prostanoids in the rat is uncertain. Prostaglandins 59-70 cytochrome c oxidase II, mitochondrial Rattus norvegicus 21-26 12900348-3 2003 In the present study, the hypothesis that synthesis of vasoactive prostanoids via the COX-2 pathway can alter pulmonary and systemic vascular resistance was investigated, and the effects of selective COX-2 inhibitors on pulmonary and systemic responses to the prostanoid precursor arachidonic acid were examined in the anesthetized rat with a recently developed right-heart catheterization technique. Prostaglandins 66-77 cytochrome c oxidase II, mitochondrial Rattus norvegicus 86-91 12735864-1 2003 Cyclooxygenase, the rate-limiting enzyme in the production of prostaglandins, exists in two isoforms, the constitutive cyclooxygenase 1 (Cox-1) and the inducible cyclooxygenase 2 (Cox-2). Prostaglandins 62-76 cytochrome c oxidase II, mitochondrial Rattus norvegicus 180-185 12673493-11 2003 CONCLUSION: These data show that COX-1 and COX-2 derived prostaglandins induced by low concentration AA pretreatment reduce the colonic mucosal injury and the increase in the MPO activity in colitis, respectively. Prostaglandins 57-71 cytochrome c oxidase II, mitochondrial Rattus norvegicus 43-48 12621123-10 2003 Our data thus indicate that intrapulmonary meconium up-regulates lung COX-2 and NOS-2 gene expression, suggesting an important role for prostaglandins and nitric oxide in the meconium aspiration-induced pulmonary inflammation and hemodynamic changes. Prostaglandins 136-150 cytochrome c oxidase II, mitochondrial Rattus norvegicus 70-75 12672535-3 2003 COX-1 is generally considered to contribute to cell homeostasis, whereas COX-2 is thought to mediate inflammatory/immune PG formation. Prostaglandins 121-123 cytochrome c oxidase II, mitochondrial Rattus norvegicus 73-78 12674222-1 2003 The aim of the present study was to determine the effect of social stress and significance of prostaglandins (PG) generated by constitutive and inducible cyclooxygenase (COX-1 and COX-2) in the stimulation of hypothalamic-pituitary-adrenal (HPA) axis by corticotropin releasing hormone (CRH) under basal and social crowding stress conditions. Prostaglandins 94-108 cytochrome c oxidase II, mitochondrial Rattus norvegicus 180-185 12674222-1 2003 The aim of the present study was to determine the effect of social stress and significance of prostaglandins (PG) generated by constitutive and inducible cyclooxygenase (COX-1 and COX-2) in the stimulation of hypothalamic-pituitary-adrenal (HPA) axis by corticotropin releasing hormone (CRH) under basal and social crowding stress conditions. Prostaglandins 110-112 cytochrome c oxidase II, mitochondrial Rattus norvegicus 180-185 12643859-9 2003 CONCLUSION: In addition to NO synthesized by constitutive NOS (cNOS), prostaglandins produced by both COX-1 and COX-2 participate in the pathogenesis of PI, albeit in different pathological mechanisms. Prostaglandins 70-84 cytochrome c oxidase II, mitochondrial Rattus norvegicus 112-117 12490538-1 2003 Cytosolic phospholipase A2 (cPLA2), cyclooxygenase-1 (COX-1), and cyclooxygenase-2 (COX-2) regulate the formation of physiologically active prostaglandins, the production of which is known to be elevated in several renal disorders. Prostaglandins 140-154 cytochrome c oxidase II, mitochondrial Rattus norvegicus 84-89 14558438-9 2003 Furthermore the most potent compounds 2 g and 3 g from each series were screened in vitro for inhibition of both COX-2 and COX-1 catalysed prostaglandin biosynthesis (radiochemical assay). Prostaglandins 139-152 cytochrome c oxidase II, mitochondrial Rattus norvegicus 113-118 12120902-4 2002 In the present studies an involvement of adrenergic system and prostaglandins synthesized by constitutive cyclooxygenase (COX-1) and inducible cyclooxygenase (COX-2) in the nicotine-induced HPA response in rats was investigated. Prostaglandins 63-77 cytochrome c oxidase II, mitochondrial Rattus norvegicus 159-164 12499663-2 2002 Cyclooxygenase (COX) -2, a rate-limiting enzyme for prostanoid synthesis, is also induced by ischemia. Prostaglandins 52-62 cytochrome c oxidase II, mitochondrial Rattus norvegicus 0-23 12193539-1 2002 Prostanoids are arachidonic acid (AA) metabolites derived from the cyclooxygenase (COX1 and COX2 isozymes) pathway and are involved in signal transduction pathways activated by distinct ILs. Prostaglandins 0-11 cytochrome c oxidase II, mitochondrial Rattus norvegicus 92-96 12369741-25 2002 Social stress markedly diminishes the mediation of PGs generated by COX-1 but PGs synthesized by COX-2 do not substantially participate in the carbachol-induced HPA response. Prostaglandins 78-81 cytochrome c oxidase II, mitochondrial Rattus norvegicus 97-102 12410334-1 2002 Prostanoid synthesis is regulated by the enzyme cyclo-oxygenase (COX) that is present in at least two isoforms: COX-1, the constitutive form, and COX-2, the inducible form. Prostaglandins 0-10 cytochrome c oxidase II, mitochondrial Rattus norvegicus 146-151 12181171-7 2002 These results suggest that generation of endothelial vasodilator prostanoids, from COX-1 and COX-2 isoforms, accounts for the increased mesenteric blood flow in portal hypertension. Prostaglandins 65-76 cytochrome c oxidase II, mitochondrial Rattus norvegicus 93-98 11782374-2 2002 iNOS may regulate COX-2 production of proinflammatory prostaglandins, which are known to play a key role in colon tumor development. Prostaglandins 54-68 cytochrome c oxidase II, mitochondrial Rattus norvegicus 18-23 11834525-12 2002 In conclusion, PCS gene transfer modulated COX-2-mediated prostanoid synthesis and inhibited neointimal formation after balloon injury. Prostaglandins 58-68 cytochrome c oxidase II, mitochondrial Rattus norvegicus 43-48 11861316-3 2002 Since PG synthesis is mediated by cyclooxygenase-1 and -2 (COX-1 and COX-2), the present study was designed to examine which COX isoform is involved in this phenomenon. Prostaglandins 6-8 cytochrome c oxidase II, mitochondrial Rattus norvegicus 69-74 11918652-3 2002 In the present study, 2 and 4 weeks following partial sciatic nerve ligation (PSNL), we observed a dramatic increase in the prostaglandin synthesizing enzyme cyclooxygenase (COX)2-immunoreactive (IR) cell profiles in the injury site and adjacent region. Prostaglandins 124-137 cytochrome c oxidase II, mitochondrial Rattus norvegicus 174-179 11882689-14 2002 Prostaglandin production via COX-2 appears to mediate the development of acute inflammatory hyperaemia, but nitrergic mechanisms may supervene subsequently. Prostaglandins 0-13 cytochrome c oxidase II, mitochondrial Rattus norvegicus 29-34 11834525-3 2002 We hypothesized that overexpression of PCS may modulate COX-2-mediated prostaglandin (PG) metabolism. Prostaglandins 71-84 cytochrome c oxidase II, mitochondrial Rattus norvegicus 56-61 11834525-3 2002 We hypothesized that overexpression of PCS may modulate COX-2-mediated prostaglandin (PG) metabolism. Prostaglandins 86-89 cytochrome c oxidase II, mitochondrial Rattus norvegicus 56-61 11805196-1 2002 Prostaglandin formation is enhanced in vascular disease, in part through induction of cyclooxygenase (COX-2) in vascular smooth muscle cells. Prostaglandins 0-13 cytochrome c oxidase II, mitochondrial Rattus norvegicus 102-107 11795877-1 2002 COX-2 is rapidly expressed by various stimuli and plays a key role in conversion of free arachidonic acid to prostaglandins (PGs). Prostaglandins 109-123 cytochrome c oxidase II, mitochondrial Rattus norvegicus 0-5 11795877-1 2002 COX-2 is rapidly expressed by various stimuli and plays a key role in conversion of free arachidonic acid to prostaglandins (PGs). Prostaglandins 125-128 cytochrome c oxidase II, mitochondrial Rattus norvegicus 0-5 11853230-1 2002 Inducible nitric oxide synthase (iNOS) and cyclooxygenase (COX)-2 are expressed in vascular smooth muscle cells stimulated with interleukin-1beta (IL-1beta), resulting in the production of nitric oxide (NO) and prostaglandins (PGs) such as PGI2. Prostaglandins 211-225 cytochrome c oxidase II, mitochondrial Rattus norvegicus 43-65 11853230-1 2002 Inducible nitric oxide synthase (iNOS) and cyclooxygenase (COX)-2 are expressed in vascular smooth muscle cells stimulated with interleukin-1beta (IL-1beta), resulting in the production of nitric oxide (NO) and prostaglandins (PGs) such as PGI2. Prostaglandins 227-230 cytochrome c oxidase II, mitochondrial Rattus norvegicus 43-65 11785774-1 2001 The involvement of prostaglandins synthesized by constitutive (COX-1) and inducible cyclooxygenase (COX-2) in central stimulation of the hypothalamic-pituitary-adrenal (HPA) axis by adrenergic receptor agonists was investigated in conscious rats. Prostaglandins 19-33 cytochrome c oxidase II, mitochondrial Rattus norvegicus 100-105 11805196-7 2002 Both the COX-1 inhibitor SC-560 and the COX-2 inhibitor SC-236 suppressed the generation of PGE(2) and PGF(2alpha), particularly when combined, suggesting a role for both isozymes in the generation of prostaglandins in this model. Prostaglandins 201-215 cytochrome c oxidase II, mitochondrial Rattus norvegicus 40-45 11785775-1 2001 The purpose of the present study was to investigate the contribution of prostaglandins (PGs) synthesized by constitutive (COX-1) and inducible (COX-2) cyclooxygenase to stimulation of the hypothalamic-pituitary-adrenal (HPA) axis by adrenergic receptor agonists in rats under social crowing stress 3 days, (21 per a cage for 6) animals. Prostaglandins 72-86 cytochrome c oxidase II, mitochondrial Rattus norvegicus 144-149 11785775-1 2001 The purpose of the present study was to investigate the contribution of prostaglandins (PGs) synthesized by constitutive (COX-1) and inducible (COX-2) cyclooxygenase to stimulation of the hypothalamic-pituitary-adrenal (HPA) axis by adrenergic receptor agonists in rats under social crowing stress 3 days, (21 per a cage for 6) animals. Prostaglandins 88-91 cytochrome c oxidase II, mitochondrial Rattus norvegicus 144-149 11703585-6 2001 RESULTS: Induction of COX-2 mRNA expression due to furosemide was paralleled by increased renal excretion of prostanoids. Prostaglandins 109-120 cytochrome c oxidase II, mitochondrial Rattus norvegicus 22-27 11758826-1 2001 Two isoenzymes of cyclooxygenase (COX), the key enzyme in prostaglandin (PG) biosynthesis, COX-1 and COX-2, have been identified. Prostaglandins 58-76 cytochrome c oxidase II, mitochondrial Rattus norvegicus 101-106 11703397-5 2001 Prostanoid synthesis is regulated by the enzyme cyclo-oxygenase (COX), which is present in at least two isoforms, COX-1 (the constitutive form) and COX-2 (the inducible form). Prostaglandins 0-10 cytochrome c oxidase II, mitochondrial Rattus norvegicus 148-153 11785783-7 2001 These results suggest that FR140423 shows a potent anti-inflammatory effect mediated by inhibition of prostanoids produced by COX-2 in inflamed tissues immunized with type II collagen, with a greatly improved safety profile compared to indomethacin. Prostaglandins 102-113 cytochrome c oxidase II, mitochondrial Rattus norvegicus 126-131 11703585-11 2001 CONCLUSIONS: These findings suggest that COX-2-derived prostanoids are of major relevance in modulating the renal effects of diuretics. Prostaglandins 55-66 cytochrome c oxidase II, mitochondrial Rattus norvegicus 41-46 11565600-13 2001 Our results suggest that therapeutic approaches based on long-term blocking including COX-1, might be superior to selective COX-2 blocking to suppress the local synthesis of prostanoids. Prostaglandins 174-185 cytochrome c oxidase II, mitochondrial Rattus norvegicus 124-129 11597589-14 2001 )-induced hyperalgesia is mediated predominantly through a COX-2 induced prostanoids in the POA and the DBB in rats. Prostaglandins 73-84 cytochrome c oxidase II, mitochondrial Rattus norvegicus 59-64 11511527-5 2001 Maximal expression of COX-2 was detected 16 h after PH with increased levels present even at 96 h. Pharmacological inhibition of COX-2 activity with NS398 shunted the up-regulation of cell proliferation after PH, which suggests a positive interaction of prostaglandins with the progression of the cell cycle. Prostaglandins 254-268 cytochrome c oxidase II, mitochondrial Rattus norvegicus 22-27 11511527-5 2001 Maximal expression of COX-2 was detected 16 h after PH with increased levels present even at 96 h. Pharmacological inhibition of COX-2 activity with NS398 shunted the up-regulation of cell proliferation after PH, which suggests a positive interaction of prostaglandins with the progression of the cell cycle. Prostaglandins 254-268 cytochrome c oxidase II, mitochondrial Rattus norvegicus 129-134 11285308-8 2001 In conclusion, we documented an increase in renal cortical COX-2 protein expression associated with a different renal hemodynamic response to selective systemic COX-2 inhibition in D as compared with C animals, indicating a role of COX-2-derived PG in pathological renal hemodynamic changes in diabetes. Prostaglandins 246-248 cytochrome c oxidase II, mitochondrial Rattus norvegicus 59-64 11470756-5 2001 The key enzymes of prostaglandin synthesis, cyclooxygenase I (Cox-1) and II (Cox-2), were present in all unaltered and preneoplastic cells and tended to decrease in the later stages of hepatocarcinogenesis. Prostaglandins 19-32 cytochrome c oxidase II, mitochondrial Rattus norvegicus 77-82 11429387-6 2001 Upon LPS challenge cyclo-oxygenase (COX)-2 expression was enhanced, and this was paralleled by a 2 - 9-fold increase in prostanoid formation, including isoprostanes. Prostaglandins 120-130 cytochrome c oxidase II, mitochondrial Rattus norvegicus 19-42 11376495-1 2001 Prostaglandins (PG) derived from COX-1 are essential for the maintenance of mucosal integrity but COX-2 isoform synthesizes PG at a site of inflammation. Prostaglandins 124-126 cytochrome c oxidase II, mitochondrial Rattus norvegicus 98-103 11338378-9 2001 These results suggested that endogenous PGs generated through COX-2 may enhance the neovascularization in sponge granuloma by increased expression of VEGF and that a COX-2 inhibitor would facilitate the management of conditions involving angiogenesis. Prostaglandins 40-43 cytochrome c oxidase II, mitochondrial Rattus norvegicus 62-67 11338378-9 2001 These results suggested that endogenous PGs generated through COX-2 may enhance the neovascularization in sponge granuloma by increased expression of VEGF and that a COX-2 inhibitor would facilitate the management of conditions involving angiogenesis. Prostaglandins 40-43 cytochrome c oxidase II, mitochondrial Rattus norvegicus 166-171 10861857-7 2000 Furthermore, ebselen inhibits LPS-induced COX-2 expression, which is responsible for proinflammatory prostaglandin production, without affecting constitutive COX-1 expression. Prostaglandins 101-114 cytochrome c oxidase II, mitochondrial Rattus norvegicus 42-47 11549833-16 2001 CONCLUSIONS: (1) Growth factors accelerate ulcer healing due to enhancement in the microcirculation around the ulcer and these effects are specific because they can be abolished by neutralization with antibodies; (2) COX-2-derived prostaglandins and suppression of gastric secretion may play an important role in the acceleration of ulcer healing by various growth factors, and (3) the local effects of EGF, HGF and bFGF on ulcer healing can be reproduced by their systemic application indicating the high efficacy of growth factors to accelerate this healing. Prostaglandins 231-245 cytochrome c oxidase II, mitochondrial Rattus norvegicus 217-222 11192947-14 2000 We conclude that 1) neutralization of HGF and gastrin by their specificantibodies delays ulcer healing due fall in the microcirculation around the ulcer and a decrease in the COX-2 expression, 2) COX-2 derived prostaglandins may play an important role in acceleration of the ulcer healing by various growth factors including HGF and gastrin, 3) enhancement of the local pool for growth factors such as HGF and gastrin at the ulcer site could offer a new modality for treatment of gastric ulcer. Prostaglandins 210-224 cytochrome c oxidase II, mitochondrial Rattus norvegicus 196-201 11094044-9 2000 Both nonselective inhibition of Cox by indomethacin and selective inhibition of the inducible Cox-2 by NS-398 abolished prostanoid release. Prostaglandins 120-130 cytochrome c oxidase II, mitochondrial Rattus norvegicus 94-99 10821793-12 2000 These results suggested that COX-2 may enhance bFGF-induced neovascularization in sponge granuloma by PG-mediated expression of VEGF, and that a COX-2 inhibitor would facilitate the management of conditions involving angiogenesis. Prostaglandins 102-104 cytochrome c oxidase II, mitochondrial Rattus norvegicus 29-34 10801275-2 2000 Cyclooxygenase (COX), the rate-limiting enzyme for prostaglandin synthesis, exists in two isoforms, COX-1 and COX-2. Prostaglandins 51-64 cytochrome c oxidase II, mitochondrial Rattus norvegicus 110-115 11595412-3 2001 Prostaglandin biosynthesis is catalysed by the enzyme cyclooxygenase (COX), which exists in two isoforms, COX-1 and COX-2. Prostaglandins 0-13 cytochrome c oxidase II, mitochondrial Rattus norvegicus 116-121 11595412-4 2001 Initially the concept was developed that COX-1 functions as housekeeping enzyme, whereas COX-2 yields prostaglandins involved in pathophysiological reactions such as inflammation. Prostaglandins 102-116 cytochrome c oxidase II, mitochondrial Rattus norvegicus 89-94 10751353-1 2000 Cyclooxygenase (Cox), the key enzyme of prostanoid synthesis, consists of the two isoforms Cox-1 and Cox-2, both recently noted to be constitutively expressed in rat lungs with a distinct profile of cellular distribution. Prostaglandins 40-50 cytochrome c oxidase II, mitochondrial Rattus norvegicus 101-106 10882189-3 2000 These results suggest that there is an interaction between IL1alpha, NO and prostaglandins and that are involved COX-2 and iNOS in this interrelationship. Prostaglandins 76-90 cytochrome c oxidase II, mitochondrial Rattus norvegicus 113-118 10807499-1 2000 OBJECTIVE AND DESIGN: To investigate the effect of JTE-522, a selective cyclooxygenase (COX)-2 inhibitor, on prostaglandin (PG) production and COX expression in rats. Prostaglandins 109-122 cytochrome c oxidase II, mitochondrial Rattus norvegicus 72-94 10807499-8 2000 CONCLUSION: These results indicate that JTE-522 selectively inhibits PG production mediated by COX-2 in inflammatory tissues. Prostaglandins 69-71 cytochrome c oxidase II, mitochondrial Rattus norvegicus 95-100 11193597-8 2000 In conclusion, the results provide evidence that cholera toxin, in addition to other mediators, uses prostaglandin E2 to exert its secretory effect and that in the case of cholera toxin prostaglandins are metabolized via COX-2. Prostaglandins 186-200 cytochrome c oxidase II, mitochondrial Rattus norvegicus 221-226 10593866-2 1999 Therefore, we investigated whether hepatocyte growth factor (HGF) affects expression of COX-2 (the inducible form of the prostaglandin synthesizing enzyme, cyclooxygenase) in gastric epithelial cells and whether this action is mediated through the MAP (ERK) kinase signaling pathway. Prostaglandins 121-134 cytochrome c oxidase II, mitochondrial Rattus norvegicus 88-93 10674759-1 2000 Prostaglandins, potent mediators of inflammation, are generated from arachidonic acid (AA) via the action of cyclooxygenase-1 and -2 (COX-1 and COX-2). Prostaglandins 0-14 cytochrome c oxidase II, mitochondrial Rattus norvegicus 144-149 10669114-12 1999 CONCLUSIONS: These results suggest that FMLP, presumably acting on inflammatory cells trapped in the pulmonary circulation of endotoxin treated rats, induced prostanoid formation mainly via the COX-2 pathway, and that its inhibition by NS-398 had no detectable potentiating effect on LTB4 or cysteinyl-LT biosynthesis. Prostaglandins 158-168 cytochrome c oxidase II, mitochondrial Rattus norvegicus 194-199 10584847-10 1999 These results pertaining to COX-2 mRNA agree well with the previous observations of changes in prostaglandin metabolism induced by focal cerebral ischemia. Prostaglandins 95-108 cytochrome c oxidase II, mitochondrial Rattus norvegicus 28-33 10537081-6 1999 These observations indicated that IL-1beta induced the release of SP from the DRG cells via specific IL-1 receptors, the mechanism of which might involve prostanoid systems produced by COX-2. Prostaglandins 154-164 cytochrome c oxidase II, mitochondrial Rattus norvegicus 185-190 10718107-3 1999 While the effect of EGF is abolished by L-NMMA, an NO antagonist, the NS-398, a cyclooxygenase-II (COX-II) inhibitor, prevents the augmentation of prostanoids induced by EGF. Prostaglandins 147-158 cytochrome c oxidase II, mitochondrial Rattus norvegicus 80-97 10718107-3 1999 While the effect of EGF is abolished by L-NMMA, an NO antagonist, the NS-398, a cyclooxygenase-II (COX-II) inhibitor, prevents the augmentation of prostanoids induced by EGF. Prostaglandins 147-158 cytochrome c oxidase II, mitochondrial Rattus norvegicus 99-105 10718107-4 1999 These results suggest that there is an interaction among EGF, NO and PGs and that in this interrelationship are involved COX-II and iNOS. Prostaglandins 69-72 cytochrome c oxidase II, mitochondrial Rattus norvegicus 121-127 10502281-3 1999 The purpose of this study is to examine the expression of the key enzymes in prostaglandin synthesis: cyclooxygenase-1 (COX-1, constitutive) and cyclooxygenase-2 (COX-2, inducible), during phagocytosis of ROS by RPE cells. Prostaglandins 77-90 cytochrome c oxidase II, mitochondrial Rattus norvegicus 163-168 10674917-11 1999 The early phase is mediated mainly by COX-1/PGs, while the later phase is mediated by iNOS/NO, in addition to prostaglandins (PGs) produced by both COX-1 and COX-2. Prostaglandins 126-129 cytochrome c oxidase II, mitochondrial Rattus norvegicus 158-163 10502281-8 1999 Induction of COX-2 by ROS phagocytosis and growth factors through the modulation of prostanoid synthesis may play an important role in the regulation of cell functions associated with photoreceptor cell renewal. Prostaglandins 84-94 cytochrome c oxidase II, mitochondrial Rattus norvegicus 13-18 10422661-24 1999 These findings suggest that spinal prostanoids produced via both COX1 and COX2 pathways may play a role in neuropathic pain states and suggest the clinical utility of opioid plus COX-inhibitor combination therapy. Prostaglandins 35-46 cytochrome c oxidase II, mitochondrial Rattus norvegicus 74-78 10371510-11 1999 Thus, COX 2 may be pro-inflammatory during the early phase of a carrageenin-induced pleurisy, dominated by polymorphonuclear leucocytes, but may aid resolution at the later, mononuclear cell-dominated phase by generating an alternative set of anti-inflammatory prostaglandins. Prostaglandins 261-275 cytochrome c oxidase II, mitochondrial Rattus norvegicus 6-11 9736824-17 1998 Our data demonstrate that a Cox 2 selective inhibitor of prostaglandin formation, flosulide, has beneficial effects on preservation of kidney function in rats with PHN, whereas aspirin has not. Prostaglandins 57-70 cytochrome c oxidase II, mitochondrial Rattus norvegicus 28-33 10235299-2 1999 Prostaglandin synthesis is catalyzed by cyclooxygenase (COX; prostaglandin synthase) which occurs as two isozymes, COX-1 and COX-2. Prostaglandins 0-13 cytochrome c oxidase II, mitochondrial Rattus norvegicus 125-130 9834273-1 1998 BACKGROUND & AIMS: The cyclooxygenase (COX) enzymes catalyze the initial step of prostaglandin formation; the inducible form, COX-2, plays a role in inflammation. Prostaglandins 85-98 cytochrome c oxidase II, mitochondrial Rattus norvegicus 130-135 9988750-4 1999 Cyclooxygenase (COX) the rate-limiting enzyme in PG biosynthesis has two isoforms, the constitutive COX-1 and an inducible COX-2. Prostaglandins 49-51 cytochrome c oxidase II, mitochondrial Rattus norvegicus 123-128 9698346-8 1998 We present a hypothesis that IL-1 induces SWS, at least in part, via COX-2-mediated PG production in the PGD2-SZ. Prostaglandins 84-86 cytochrome c oxidase II, mitochondrial Rattus norvegicus 69-74 9726391-14 1998 CONCLUSIONS: (i) Gastric adaptation to aspirin injury involves enhanced cell proliferation which appears to be mediated by increased expression of SP and TGF alpha, and (ii) rapid upregulation of COX-2 expression following single and repeated ASA insults may represent a compensatory response to suppression of prostaglandin generation by this NSAID. Prostaglandins 311-324 cytochrome c oxidase II, mitochondrial Rattus norvegicus 196-201 9681442-3 1998 The synthesis of prostaglandins depends upon the production and conversion of arachidonic acid, steps that are catalyzed by phospholipase A2 (PLA2) and cyclooxygenase (COX), respectively. Prostaglandins 17-31 cytochrome c oxidase II, mitochondrial Rattus norvegicus 168-171 10189071-3 1998 These results suggest that there is an interaction between IL-1alpha, NO and prostaglandins and that this interrelationship involves COX-2. Prostaglandins 77-91 cytochrome c oxidase II, mitochondrial Rattus norvegicus 133-138 9649464-1 1998 BACKGROUND & AIMS: Selective inhibitors of cyclooxygenase (COX)-2 are being developed as gastrointestinal-sparing anti-inflammatory drugs based on the premise that this isoform is solely responsible for prostaglandin synthesis at sites of inflammation, whereas COX-1 produces prostaglandins important for maintenance of mucosal integrity. Prostaglandins 207-220 cytochrome c oxidase II, mitochondrial Rattus norvegicus 47-69 9649464-1 1998 BACKGROUND & AIMS: Selective inhibitors of cyclooxygenase (COX)-2 are being developed as gastrointestinal-sparing anti-inflammatory drugs based on the premise that this isoform is solely responsible for prostaglandin synthesis at sites of inflammation, whereas COX-1 produces prostaglandins important for maintenance of mucosal integrity. Prostaglandins 280-294 cytochrome c oxidase II, mitochondrial Rattus norvegicus 47-69 9649464-7 1998 The degree of suppression of prostaglandin synthesis at the site of inflammation correlated significantly with inhibition of COX-1 but not COX-2. Prostaglandins 29-42 cytochrome c oxidase II, mitochondrial Rattus norvegicus 139-144 9649464-9 1998 To achieve desirable anti-inflammatory effects, COX-2 inhibitors needed to be given at doses in which selectivity was lost, leading to suppression of gastric prostaglandin synthesis and to mucosal injury. Prostaglandins 158-171 cytochrome c oxidase II, mitochondrial Rattus norvegicus 48-53 9561138-2 1997 Cyclooxygenase isozymes Cox-1 and Cox-2 as enzymes essential for prostaglandin biosynthesis were therefore investigated in rat spinal cord. Prostaglandins 65-78 cytochrome c oxidase II, mitochondrial Rattus norvegicus 34-39 9533935-1 1998 Prostanoid generation may proceed via both isoforms of cyclooxygenase, Cox-1 and Cox-2. Prostaglandins 0-10 cytochrome c oxidase II, mitochondrial Rattus norvegicus 81-86 9568691-3 1998 IL-1beta also induces the coexpression of the inducible isoform of cyclooxygenase (COX-2) that results in the overproduction of proinflammatory prostaglandins. Prostaglandins 144-158 cytochrome c oxidase II, mitochondrial Rattus norvegicus 83-88 9559932-1 1998 Non-steroidal anti-inflammatory drugs inhibit constitutive (COX-1) and induced cyclooxygenase (COX-2), blocking prostaglandin production. Prostaglandins 112-125 cytochrome c oxidase II, mitochondrial Rattus norvegicus 95-100 9530264-10 1998 Divergent regulation of COX-2 in cortex and medulla by dietary salt suggests that prostaglandins in different kidney regions serve different functions, with medullary production playing a role in promoting the excretion of salt and water in volume overload, whereas cortical prostaglandins may protect glomerular circulation in volume depletion. Prostaglandins 82-96 cytochrome c oxidase II, mitochondrial Rattus norvegicus 24-29 9530264-10 1998 Divergent regulation of COX-2 in cortex and medulla by dietary salt suggests that prostaglandins in different kidney regions serve different functions, with medullary production playing a role in promoting the excretion of salt and water in volume overload, whereas cortical prostaglandins may protect glomerular circulation in volume depletion. Prostaglandins 275-289 cytochrome c oxidase II, mitochondrial Rattus norvegicus 24-29 9513902-7 1998 These findings indicate that prostanoids generated through induction of COX-1, COX-2, and cPLA2 are implicated in the mediation of the mesangial cell injury model. Prostaglandins 29-40 cytochrome c oxidase II, mitochondrial Rattus norvegicus 79-84 9453538-1 1998 The aim of this study was to investigate the influence of the acute-phase response and the proinflammatory cytokines on the transcription of the genes encoding the limiting enzymes for the production of prostaglandins, cyclooxygenase (COX)-1 and COX-2, in the rat brain. Prostaglandins 203-217 cytochrome c oxidase II, mitochondrial Rattus norvegicus 246-251 9663836-13 1997 CONCLUSIONS: These results demonstrate a rapid up-regulation of COX-2 expression in response to aspirin, possibly representing a compensatory response to inhibition of gastric prostaglandin synthesis. Prostaglandins 176-189 cytochrome c oxidase II, mitochondrial Rattus norvegicus 64-69 12160205-3 1997 Cyclooxygenase (COX), which acts in the synthesis of PG from arachidonic acid, has been recently revealed to have two subtypes, a constitutive type (COX-1) and an inducible one (COX-2). Prostaglandins 53-55 cytochrome c oxidase II, mitochondrial Rattus norvegicus 178-183 9350647-10 1997 Cortical COX II-mediated prostaglandin formation is probably important in low salt states whereas medullary COX I-produced prostaglandins seem to be more important for renal adaptation to a high salt intake. Prostaglandins 25-38 cytochrome c oxidase II, mitochondrial Rattus norvegicus 9-15 9228016-3 1997 Cyclooxygenase (COX), the enzyme responsible for prostanoid production, exists as two isoforms: constitutive COX-1 and inducible COX-2. Prostaglandins 49-59 cytochrome c oxidase II, mitochondrial Rattus norvegicus 129-134 9554800-8 1998 The enhanced response is associated with the induced release of vasoconstrictor prostanoids sensitive to the inhibitory effect of NS-398, a preferential inhibitor of COX-2. Prostaglandins 80-91 cytochrome c oxidase II, mitochondrial Rattus norvegicus 166-171 9414024-8 1997 These results suggest that COX-2 induced in the sponge granuloma tissues may participate in neovascularization through prostaglandin formation. Prostaglandins 119-132 cytochrome c oxidase II, mitochondrial Rattus norvegicus 27-32 9323006-11 1997 The presence of COX-2 in TAL (a tubular segment postulated to be devoid of COX-1) may contribute to the handling of ions through local production of prostaglandins. Prostaglandins 149-163 cytochrome c oxidase II, mitochondrial Rattus norvegicus 16-21 9207278-11 1997 These prostaglandins were produced via COX-1, which like COX-2, is induced by endotoxin administration. Prostaglandins 6-20 cytochrome c oxidase II, mitochondrial Rattus norvegicus 57-62 9168966-1 1997 Prostaglandin (PG) synthesis during inflammation occurs mainly via the transcriptionally regulated cyclooxygenase, COX-2. Prostaglandins 0-13 cytochrome c oxidase II, mitochondrial Rattus norvegicus 115-120 9168966-1 1997 Prostaglandin (PG) synthesis during inflammation occurs mainly via the transcriptionally regulated cyclooxygenase, COX-2. Prostaglandins 15-17 cytochrome c oxidase II, mitochondrial Rattus norvegicus 115-120 9561138-10 1997 Cox-2 might therefore be regarded as the Cox isozyme responsible for increased spinal prostanoid release in nociceptive processing under peripheral stimulation. Prostaglandins 86-96 cytochrome c oxidase II, mitochondrial Rattus norvegicus 0-5 8637870-5 1996 COX-2 is a rate-limiting enzyme in prostanoid synthesis and its expression is rapidly regulated in developing and adult forebrain by physiological synaptic activity. Prostaglandins 35-45 cytochrome c oxidase II, mitochondrial Rattus norvegicus 0-5 8875635-1 1996 The synthesis of prostaglandins in the uterus at term are modulated by two isoforms of the enzyme cyclooxygenase (COX): constitutive COX-1 and inducible COX-2. Prostaglandins 17-31 cytochrome c oxidase II, mitochondrial Rattus norvegicus 153-158 8840961-2 1996 One of the mechanisms by which nonsteroidal antiinflammatory agents inhibit colon carcinogenesis is through the inhibition of prostaglandin production by cyclooxygenase isozymes (COX-1 and COX-2). Prostaglandins 126-139 cytochrome c oxidase II, mitochondrial Rattus norvegicus 189-194 8706851-6 1996 COX-2 might therefore be regarded as the COX isozyme responsible for spinal PG release in nociceptive processing under a peripheral inflammatory stimulus. Prostaglandins 76-78 cytochrome c oxidase II, mitochondrial Rattus norvegicus 0-5 8647962-4 1996 PG production was associated with upregulation of COX-2 mRNA and protein in the affected paws. Prostaglandins 0-2 cytochrome c oxidase II, mitochondrial Rattus norvegicus 50-55 8777837-4 1996 Cyclo-oxygenase (COX, prostaglandin G/H synthase) is a key enzyme in prostaglandin synthesis and has two isoforms (COX-1 and COX-2). Prostaglandins 22-35 cytochrome c oxidase II, mitochondrial Rattus norvegicus 125-130 8637870-9 1996 These results suggest that COX-2, and its diffusible prostanoid products, may play a role in postsynaptic signaling of excitatory neurons in cortex and associated structures. Prostaglandins 53-63 cytochrome c oxidase II, mitochondrial Rattus norvegicus 27-32 7706475-2 1995 Cyclooxygenase (COX) is a rate-limiting enzyme in prostanoid biosynthesis, and its recently cloned inducible form, COX-2, is induced by proinflammatory cytokines. Prostaglandins 50-60 cytochrome c oxidase II, mitochondrial Rattus norvegicus 115-120 7759893-11 1995 PAF-dependent up-regulation of COX-2 expression may constitute a novel element in the interrelationship between PAF and prostanoids in the context of allergic, inflammatory, and immune processes. Prostaglandins 120-131 cytochrome c oxidase II, mitochondrial Rattus norvegicus 31-36 7890656-2 1995 Thus, COX-2 instead of COX-1 is implicated to produce prostanoids mediating inflammatory responses. Prostaglandins 54-65 cytochrome c oxidase II, mitochondrial Rattus norvegicus 6-11 8132578-12 1994 The findings suggest that the prostanoid responses after vascular injury are, in part, mediated by acute increases in cox2 mRNA and cyclooxygenase-2 protein. Prostaglandins 30-40 cytochrome c oxidase II, mitochondrial Rattus norvegicus 118-122 8140262-0 1994 NS-398, a new anti-inflammatory agent, selectively inhibits prostaglandin G/H synthase/cyclooxygenase (COX-2) activity in vitro. Prostaglandins 60-73 cytochrome c oxidase II, mitochondrial Rattus norvegicus 103-108 8352945-9 1993 Our studies indicate that COX-2 expression may be important in regulating prostaglandin signaling in brain. Prostaglandins 74-87 cytochrome c oxidase II, mitochondrial Rattus norvegicus 26-31 1464605-8 1992 These results indicate that increased synthesis of prostaglandins and thromboxanes in lipopolysaccharide-stimulated macrophages results from selective expression of COX-2. Prostaglandins 51-65 cytochrome c oxidase II, mitochondrial Rattus norvegicus 165-170