PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
21376132-6	2011	Obtained results show that inhibition of synthesis and action of progesterone caused attenuated COX-2/PGE(2) system and dysregulated mitotic response of granulosa cells, resulting in decreased ovulation.	Dinoprostone	102-108	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	96-101	
22038825-0	2012	Prophylactic and therapeutic benefits of COX-2 inhibitor on motility dysfunction in bowel obstruction: roles of PGE2 and EP receptors.	Dinoprostone	112-116	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	41-46	
22116053-11	2012	In the brain, an expression of cytokines (TNFalpha, IL-1beta, and IL-6) and inducible forms of enzymes for prostaglandin E2 synthesis (COX-2 and mPGES) occurred, which was accompanied by a moderate activation of the transcription factors NFkappaB and STAT3, and a strong activation of the transcription factor NF-IL6, in cells of specific areas with an open blood-brain barrier.	Dinoprostone	107-123	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	135-140	
21871944-5	2011	1S-isomer of BF reduced the expression of genes P450scc, StAR, PBR and DBI, as well as COX-2, which are involved in regulating the rate-limiting steps of progesterone or PGE2 biosynthesis.	Dinoprostone	170-174	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	87-92	
21741371-3	2011	Thus, COX-1 is constitutive and expressed ubiquitously and serves a housekeeping role, while COX-2 is inducible or upregulated by inflammatory/injury stimuli such as interleukin-1beta, tumor necrosis factor-alpha, and lipopolysaccharide in macrophage, monocyte, synovial, liver, and lung, and is associated with prostaglandin E2 and prostacyclin production that evokes or sustains systemic/peripheral inflammatory symptoms.	Dinoprostone	312-328	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	93-98	
20549385-6	2011	Treatment with either COX-1 or COX-2 selective inhibitor or their combination equally decreased the level of TNF-alpha, PGE2, and cleaved caspase-3 and attenuated astrogliosis and neuronal cell loss.	Dinoprostone	120-124	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	31-36	
20549385-8	2011	These results indicate that the activity of both isoforms is detrimental in neuroinflammatory conditions associated with Abeta, but COX-1 activity is necessary for COX-2 induction and COX-2 activity seems to be the main source of PGE2 increment.	Dinoprostone	230-234	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	184-189	
21551240-4	2011	The development of mechanical and thermal hyperalgesia and increased production of PGE(2) was blocked by NS-398 (15-150 ng), a selective COX-2 inhibitor.	Dinoprostone	83-89	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	137-142	
22436072-9	2012	ACh-stimulated TxB2 was higher in all O-DR. ACh-stimulated PGE2 release was increased in arteries from 6- and 12-month-old O-DR, whereas PGF(2alpha) was increased only in 12-month-old O-DR. COX-2, but not COX-1, expression was higher in O-DR than O-CR.	Dinoprostone	59-63	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	190-195	
22060288-7	2011	By contrast, dmPGE(2) pretreatment significantly exacerbated tissue injury and simultaneously increased COX-2 expression, PGE(2) levels and MPO activity in RE-rats.	Dinoprostone	15-21	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	104-109	
21394197-10	2011	Functional significance was demonstrated by prostaglandin E2 (PGE(2)) release 4 hours after stimulation with IL-1beta, which could be aborted by a selective COX-2 (parecoxib) and a non-selective COX-inhibitor (indomethacin).	Dinoprostone	62-68	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	157-162	
21394197-0	2011	IL-1beta stimulates COX-2 dependent PGE2 synthesis and CGRP release in rat trigeminal ganglia cells.	Dinoprostone	36-40	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	20-25	
20333648-10	2010	These results demonstrate that in RBA-1 cells, EV71-induced COX-2 expression associated with PGE(2) production is mediated through activation of c-Src/PDGFR/PI3K/Akt/p42/p44 MAPK to initiate the expression of AP-1.	Dinoprostone	93-99	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	60-65	
21394197-10	2011	Functional significance was demonstrated by prostaglandin E2 (PGE(2)) release 4 hours after stimulation with IL-1beta, which could be aborted by a selective COX-2 (parecoxib) and a non-selective COX-inhibitor (indomethacin).	Dinoprostone	44-60	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	157-162	
21146550-6	2011	With COX-2 selective inhibitors and ibuprofen, a return of the nociceptive response developed over time, despite complete inhibition of PGE(2) in the spinal fluid.	Dinoprostone	136-142	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	5-10	
20552550-3	2010	The expression patterns of PGE2 synthesis enzymes such as cyclooxygenase (COX)-1, COX-2 and microsomal PGE synthase (mPGES)-1, and PGE2 receptors (EP2 and EP4) were examined in cisplatin-induced rat renal failure.	Dinoprostone	27-31	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	82-87	
20610553-8	2010	Antagonist studies with SC-560 (COX-1 inhibitor) and SC-236 (COX-2 inhibitor) showed that LPS-induced PGE(2) release was generated from both COX-1 and COX-2.	Dinoprostone	102-108	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	61-66	
20610553-8	2010	Antagonist studies with SC-560 (COX-1 inhibitor) and SC-236 (COX-2 inhibitor) showed that LPS-induced PGE(2) release was generated from both COX-1 and COX-2.	Dinoprostone	102-108	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	151-156	
20082628-14	2010	Furthermore, COX-2 expression was significantly elevated with indomethacin and SC-560, explaining the source of augmented PGE(2) synthesis.	Dinoprostone	122-128	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	13-18	
19754408-3	2009	Two inducible enzymes, COX-2 and microsomal prostaglandin E synthase (mPGES), regulate PGE(2) production.	Dinoprostone	87-93	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	23-28	
18786748-3	2010	Injured nerve derived cyclooxygenase 2/prostaglandin E2 (COX2/PGE2) contributes to the genesis of NeP at the early stage in young rats.	Dinoprostone	62-66	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	57-61	
18786748-4	2010	Here we show that COX2/PGE2 is involved in the maintenance of NeP at a chronic stage in aged rats.	Dinoprostone	23-27	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	18-22	
20133455-5	2010	In parallel, increases in prostaglandin-E(2) (PGE(2)) due to changes in cyclooxygenase (COX)-1 and COX-2 expression induced by the exposure of tanycytes to estradiol promote acute tanycyte plasticity.	Dinoprostone	26-44	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	99-104	
18094033-6	2008	These changes in COX-2 expression were accompanied by a 10-fold increase in COX-2 mRNA expression and a 2-fold increase in the urinary excretion of PGE2.	Dinoprostone	148-152	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	17-22	
19233864-3	2009	METHODS AND RESULTS: Western blotting, promoter assay, RT-PCR, and PGE2 immunoassay revealed that ATPgammaS induced expression of COX-2 and prostaglandin (PGE2) synthesis through the activation of p42/p44 MAPK (mitogen-activated protein kinase), p38 MAPK, and nuclear factor-kappaB (NF-kappaB).	Dinoprostone	67-71	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	130-135	
19138674-2	2009	In the current study, we investigated the molecular mechanism by which prostaglandin E(2), one of COX-2 metabolites, induces HO-1 in rat C6 brain cells.	Dinoprostone	71-89	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	98-103	
19483310-4	2009	CC06 is also a selective inhibitor of COX-2 since it can reduce prostaglandin E(2) (PGE(2)) production in the inflamed pouch dose-dependently without affecting PGE(2) production in stomach in rat air pouch model.	Dinoprostone	64-82	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	38-43	
18684886-0	2008	Calcium-sensing receptor signaling pathways in medullary thick ascending limb cells mediate COX-2-derived PGE2 production: functional significance.	Dinoprostone	106-110	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	92-97	
18684886-6	2008	Similarly, inhibition of either Gq, Gi, PKC, or CaN, which are components of the mechanism associated with CaR-stimulated COX-2-derived PGE2 synthesis, reversed the inhibitory effects of CaR on O2 consumption without affecting basal O2 consumption.	Dinoprostone	136-140	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	122-127	
18481009-4	2008	The potent compounds were evaluated for their inhibitory activities against COX-2-catalyzed PGE(2) production, with 4a, 4b and 3c showing strong inhibitory activity.	Dinoprostone	92-98	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	76-81	
18034350-11	2008	Both the COX-1,2 nonselective and COX-2 inhibitors significantly decreased PGE(2) levels to 25% of control HO levels within 24 h of the first administration, even at low dosages.	Dinoprostone	75-81	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	34-39	
18034350-13	2008	CONCLUSION: These findings suggest that although inhibitors of COX-2 or COX-1 reduced PGE(2) synthesis, only the COX-2 enzyme plays a role in the mechanism of traumatic HO.	Dinoprostone	86-92	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	63-68	
17258197-9	2007	These results suggest that COX-2-expressing cells may negatively self-regulate their functions by producing PGE2 via mPGES-1: migration into the draining lymph node and their differentiation.	Dinoprostone	108-112	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	27-32	
18344592-9	2008	The COX-2 specific inhibitor NS-398 attenuated lysoPC-stimulated DNA and protein synthesis as well as PGE(2) production by VSMCs.	Dinoprostone	102-108	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	4-9	
17988800-6	2007	PGE(2) production was correlated with altered COX-2 levels.	Dinoprostone	0-6	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	46-51	
17622965-7	2007	Controlled cortical impact (CCI) at postnatal day (PND) 17, but not PND 7, caused an additional 3-fold increase in COX-2 content and was associated with an increase in the COX-2 product PGE2.	Dinoprostone	186-190	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	172-177	
17604006-11	2007	The inhibitory effects of celecoxib and ibuprofen suggest that PGE(2) was generated via COX-2.	Dinoprostone	63-69	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	88-93	
17716650-3	2008	By solving quadratic functional analysis with prostaglandin E(2) (PGE(2)) inhibitory activities, it was calculated that involvement ratios between central and peripheral COX-2 involvement were 0.47 and 0.53 on mechanical hyperalgesia, and 0.97 and 0.03 on thermal hyperalgesia, respectively.	Dinoprostone	46-64	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	170-175	
17716650-3	2008	By solving quadratic functional analysis with prostaglandin E(2) (PGE(2)) inhibitory activities, it was calculated that involvement ratios between central and peripheral COX-2 involvement were 0.47 and 0.53 on mechanical hyperalgesia, and 0.97 and 0.03 on thermal hyperalgesia, respectively.	Dinoprostone	66-72	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	170-175	
18028778-13	2007	Liver COX-2 mRNA expression significantly increased, accompanied by an increase in liver concentrations of PGE2 and TXB2, but no obvious change in 6-K-PGF1alpha concentrations.	Dinoprostone	107-111	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	6-11	
17429720-7	2007	The expression of COX-2 mRNA in the colon was upregulated on day 3 during DSS treatment, with significant increase of prostaglandin E(2) PGE(2) production.	Dinoprostone	118-136	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	18-23	
16969135-9	2006	We found that the number of cells expressing cyclooxygenase (COX)-2, a PGE(2)-synthesizing enzyme, surged at the onset of fever in the lung and liver (but not in the brain), and that most of these cells were macrophages.	Dinoprostone	71-77	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	45-67	
16721810-5	2006	Cyclooxygenase (COX)-2 and the subsequent production of prostaglandin E2 (PGE2) were also induced by H-Ras.	Dinoprostone	56-72	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	0-22	
16721810-5	2006	Cyclooxygenase (COX)-2 and the subsequent production of prostaglandin E2 (PGE2) were also induced by H-Ras.	Dinoprostone	74-78	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	0-22	
16598755-16	2006	These findings demonstrate a coordinated induction of COX-2 and mPGES-1 by PDB/TG that proceeds through PKC/ERK and Ca2+ signaling cascades, resulting in increased PGE2 production.	Dinoprostone	164-168	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	54-59	
16933973-9	2006	It is concluded that fever is initiated by circulating PGE2 synthesized by macrophages of the LPS-processing organs (lung and liver) via phosphorylation of cPLA2 and transcriptional up-regulation of COX-2.	Dinoprostone	55-59	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	199-204	
16621493-0	2006	Elevated prostaglandin E2 level via cPLA2--COX-2--mPGES-1 pathway involved in bladder carcinogenesis induced by terephthalic acid-calculi in Wistar rats.	Dinoprostone	9-25	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	43-48	
16580130-2	2006	Short-term exposure (30 min) resulted in a small but significant amount of PGE2 release which was mainly inhibited by a selective COX-1 inhibitor, SC-560 but only partially by a selective COX-2 inhibitor, NS-398, and did not induce COX-2 protein as determined by Western blotting.	Dinoprostone	75-79	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	188-193	
16396944-5	2006	Induction of COX-2 was correlated with increased PGE2 generation, increased activation of extracellular signal-regulated kinase, decreased apoptosis, and increased cell proliferation.	Dinoprostone	49-53	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	13-18	
16396944-13	2006	Thus COX-2 and its product PGE2 may have anti-apoptotic/protective effect on GEC via the EP4 receptor of PGE2.	Dinoprostone	27-31	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	5-10	
16396944-13	2006	Thus COX-2 and its product PGE2 may have anti-apoptotic/protective effect on GEC via the EP4 receptor of PGE2.	Dinoprostone	105-109	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	5-10	
16580130-2	2006	Short-term exposure (30 min) resulted in a small but significant amount of PGE2 release which was mainly inhibited by a selective COX-1 inhibitor, SC-560 but only partially by a selective COX-2 inhibitor, NS-398, and did not induce COX-2 protein as determined by Western blotting.	Dinoprostone	75-79	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	232-237	
17048610-7	2006	2-methoxycinnamaldehyde could down-regulate them in concentration-dependently, and significant differences on the activity of COX-2 and amount of PGE2 were showed in 200 microg x mL(-1) concentration.	Dinoprostone	146-150	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	126-131	
17048610-8	2006	CONCLUSION: 2-methoxycinnamaldehyde can affect the PGE2 release in rCMEC induced by IL-1, which might be related with its inhibition on the activity of COX-2.	Dinoprostone	51-55	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	152-157	
16621493-13	2006	In conclusion, increasing PGE2 level via cPLA2--COX-2--mPGES-1 pathway may play an important role in rat bladder carcinogenesis.	Dinoprostone	26-30	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	48-53	
16490189-7	2006	On the other hand, the administration of LPS stimulated the production of prostaglandin E2/prostaglandin F2alpha and augmented the expression of COX-I 1 h after the treatment and of COX-II 2 h post-treatment.	Dinoprostone	74-90	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	182-188	
15990166-11	2006	These results suggested that induction of the COX-2-EP3 system in the placenta may be one of the causes of IUGR induced by uterine ischemia, because the EP3 receptor and PGE2 are well known to mediate vasoconstriction in many organs.	Dinoprostone	170-174	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	46-51	
16253229-3	2005	On the other hand, cyclooxygenase (COX)-2 is a key enzyme in PGE(2) production and its induction is thought to have an important role in ulcer healing.	Dinoprostone	61-67	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	19-41	
16426843-6	2006	Growth inhibition was related to COX-2 function with 90-95% reduction in PGE2 production.	Dinoprostone	73-77	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	33-38	
16724516-5	2006	BDD-11602 and rofecoxib inhibited COX-2-derived PGE(2) synthesis with IC50 values of 173 nmol/l and 169 nmol/l, respectively.	Dinoprostone	48-54	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	34-39	
17143008-8	2006	The mucosal prostaglandin E2 content in the colon showed a biphasic change, in parallel with that of the COX-2 expression.	Dinoprostone	12-28	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	105-110	
16395168-11	2006	The expression of COX-2 mRNA of anulus fibrosus cells tended to correlate to the amount of PGE2, whereas COX-2 mRNA was constitutively expressed in nucleus pulposus cells, suggesting that the roles of COX-2 might be different between nucleus pulposus and anulus fibrosus.	Dinoprostone	91-95	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	18-23	
16646980-8	2006	Although both enzymes were expressed in chondrocytes in vitro and in vivo, it appears that mainly COX-2 contributed to PGE2-dependent proliferation.	Dinoprostone	119-123	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	98-103	
16646980-16	2006	We suggest that in growth plate chondrocytes, COX-2 is responsible for PGE2 release, which stimulates cell proliferation via the EP1 receptor.	Dinoprostone	71-75	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	46-51	
16804302-11	2006	By contrast, the COX-2 expression induced by indomethacin was prevented by both PGE(2) and atropine.	Dinoprostone	80-86	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	17-22	
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.	Dinoprostone	143-147	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	56-61	
16171601-14	2005	These data also suggest that avoidance of COX-2 inhibitors can help maintain endogenous renal cortical and medullary PGE(2) synthesis and thus contribute to maintaining normal blood flow.	Dinoprostone	117-123	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	42-47	
16584974-11	2005	These results demonstrate that ethanol is capable of inhibiting FSH-induced ovarian StAR and thus, contributing to suppressed E2 secretion, at least in part, through an inhibitory action on the COX-2-PGE2 pathway.	Dinoprostone	200-204	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	194-199	
16011486-8	2005	Together, these data suggest that PGE2, synthesised in response to IL-1beta-activation of COX-2 expressing cells, directly hyperpolarises putative GABA-ergic neurones in the halo zone surrounding and projecting to the PVN, resulting in a decrease in GABA-ergic input to parvocellular neurones and consequent depolarisation.	Dinoprostone	34-38	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	90-95	
15914620-14	2005	The stimulatory action of EGF on release of PGE(2) was inhibited by the COX-2-selective inhibitor NS398.	Dinoprostone	44-50	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	72-77	
15275861-10	2004	It is suggested that the inducible production of PGE2 via COX-2 by these cells may be associated with connective tissue destruction and alveolar bone resorption.	Dinoprostone	49-53	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	58-63	
15644490-4	2005	We hypothesize that the expression of the major PGE2 synthesis enzymes cyclooxygenases 1 and 2 (COX-1, COX-2) and membrane-associated PGE2 synthase (mPGES) is altered in the kidneys of rats with NDI and CDI.	Dinoprostone	48-52	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	103-108	
15935072-4	2005	The relative contribution of the two isoforms is dynamically regulated, as the COX-2 selective inhibitor NS398 immediately prevented PGE2 and 15-F(2t)-IsoP formation during the application of NMDA, whereas the COX-1 selective inhibitor SC560 was effective only 1 h after agonist infusion.	Dinoprostone	133-137	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	79-84	
15653788-2	2005	Recent evidence that COX-2, which is expressed in postsynaptic dendritic spines, regulates PGE2 signaling in activity-dependent long-term synaptic plasticity at hippocampal perforant path-dentate granule cell synapses, suggests an important role of the COX-2-generated PGE2 in synaptic signaling.	Dinoprostone	91-95	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	21-26	
15653788-2	2005	Recent evidence that COX-2, which is expressed in postsynaptic dendritic spines, regulates PGE2 signaling in activity-dependent long-term synaptic plasticity at hippocampal perforant path-dentate granule cell synapses, suggests an important role of the COX-2-generated PGE2 in synaptic signaling.	Dinoprostone	91-95	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	253-258	
15653788-2	2005	Recent evidence that COX-2, which is expressed in postsynaptic dendritic spines, regulates PGE2 signaling in activity-dependent long-term synaptic plasticity at hippocampal perforant path-dentate granule cell synapses, suggests an important role of the COX-2-generated PGE2 in synaptic signaling.	Dinoprostone	269-273	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	21-26	
15653788-5	2005	Somatic and dendritic membrane excitability was significantly reduced when endogenous PGE2 was eliminated with a selective COX-2 inhibitor in hippocampal CA1 pyramidal neurons in slices.	Dinoprostone	86-90	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	123-128	
15653788-6	2005	Exogenous application of PGE2 produced significant increases in frequency of firing, excitatory postsynaptic potentials (EPSP) amplitude, and temporal summation in slices treated with the COX-2 inhibitor.	Dinoprostone	25-29	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	188-193	
16277686-2	2005	We investigated the kinetics of inducible cyclo-oxygenase (COX)-2 and mPGES-1 expression with respect to the production of 6-keto-PGF1alpha and PGE2 in rat chondrocytes stimulated with 10 ng/ml IL-1beta, and compared their modulation by peroxisome-proliferator-activated receptor (PPAR)gamma agonists.	Dinoprostone	144-148	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	42-65	
15678367-9	2005	Petasites extracts dose-dependently inhibited LPS-induced and thus COX-2-mediated PGE2 release in primary rat microglial cells (A: IC50= 2.4 microg/mL; C: IC50=5.8 microg/mL and D: IC50=4.6 microg/mL).	Dinoprostone	82-86	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	67-72	
15284079-7	2004	In contrast, in nuclei of brain parenchymal and endothelial cells, mPGES-1 and cPGES colocalized exclusively with COX-2 (determined by immunoblotting and immunohistochemistry); these PGESs contributed to conversion of PGH2 into PGE2.	Dinoprostone	228-232	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	114-119	
15448533-13	2004	CONCLUSION: The results of the current study suggest that NO activates COX-1 in the early phase of carrageenan and up-regulates COX-2 expression in the late phase in the skin, resulting in production of PGE2 and PGI2 at the site of inflammation, which would contribute to exacerbation of the inflammatory process.	Dinoprostone	203-207	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	128-133	
15117812-6	2004	The age-related changes in COX-2 were accompanied by a similar up-regulation in the PGE(2) synthesis.	Dinoprostone	84-90	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	27-32	
15197770-7	2004	Our data revealed suppression of COX-2 expression/PGE(2) biosynthesis.	Dinoprostone	50-56	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	33-38	
15351851-12	2004	Furthermore, since TNF-alpha is capable of inducing COX-2, inhibition of TNF-alpha production by AT might inhibit COX-2-mediated PGE(2) production.	Dinoprostone	129-134	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	114-119	
15197770-8	2004	In parallel, priming cells with 15S-HETrE resulted in greater suppression of COX-2 expression/PGE(2) biosynthesis.	Dinoprostone	94-100	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	77-82	
15373703-1	2004	Prostaglandin E2, which is produced by cyclooxygenase (COX) during arachidonic acid metabolism, is considered to be related to colon carcinogenesis and selective COX-2 inhibitors may be effective for chemoprevention without the adverse side effects of non-selective, nonsteroid anti-inflammatory drugs.	Dinoprostone	0-16	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	162-167	
15249113-5	2004	Furthermore, to determine if the reduction of brain PGE2 concentration was due only to downregulation of COX-2 protein or if it also involves the terminal PGE synthase, we determined brain microsomal PGE synthase protein level.	Dinoprostone	52-56	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	105-110	
15193428-2	2004	Synthesis of PGE2 is controlled by cyclooxygenase (COX), either the COX-1 or COX-2 isoform.	Dinoprostone	13-17	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	77-82	
14636300-13	2003	It was concluded that COX-2-dependent PGE2 is able to potentiate its effects in the kidney by up-regulating its own receptors.	Dinoprostone	38-42	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	22-27	
15193428-12	2004	These data implies that suppression of PGE2 activity may induce the expression of spinal COX-2 in Freund"s adjuvant-induced pain model.	Dinoprostone	39-43	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	89-94	
15082878-10	2004	Mucosal PGE2 content was increased following IA treatment, with apparent expression of COX-2 mRNA in the stomach, and the increased PGE2 production was significantly suppressed by SC-560 and rofecoxib as well as indomethacin.	Dinoprostone	8-12	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	87-92	
14960618-7	2004	To identify the COX isozyme contributing to this release, SC 58236, a COX-2 inhibitor, was given and found to reduce prostaglandin E2 release evoked by either agent.	Dinoprostone	117-133	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	70-75	
12881220-13	2003	Finally, HMCM-induced upregulation of COX-2 was accompanied by upregulation of PGI2 and PGE2.	Dinoprostone	88-92	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	38-43	
14623498-3	2003	Exposure of astrocytes to cytokines resulted in a time-dependent increase in PGE2 production that was marked by increased expression of secretory sPLA2 and COX-2, but not COX-1 and cytosolic cPLA2.	Dinoprostone	77-81	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	156-161	
12799304-3	2003	Unstimulated IMCD released moderate, but significant, amounts of PGE2, which were more sensitive to cyclooxygenase (COX)-2 than COX-1 inhibition.	Dinoprostone	65-69	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	100-122	
12799304-6	2003	Differential COX inhibition studies revealed that purinergic-stimulated release of PGE2 was more sensitive to a COX-1-specific inhibitor (valeroyl salicylate) than a COX-2-specific inhibitor (NS-398).	Dinoprostone	83-87	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	166-171	
12799304-7	2003	Thus purinergic stimulation resulted in significantly more release of PGE2 in the presence of COX-2 inhibitor than COX-1 inhibitor.	Dinoprostone	70-74	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	94-99	
12925151-15	2003	Rebamipide suppressed an indometacin-induced increase in gastric epithelial permeability by increasing PGE2 levels in a COX-2 dependent manner.	Dinoprostone	103-107	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	120-125	
12784118-3	2003	To assess whether COX-2 is regulated after stress, we have used adult male Wistar rats, some of which were immobilized during 6 h. An increase in PGE2 concentration occurs in brain cortex after 2-6 h of the onset of stress as well as an enhancement of COX-2 protein.	Dinoprostone	146-150	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	18-23	
12784118-3	2003	To assess whether COX-2 is regulated after stress, we have used adult male Wistar rats, some of which were immobilized during 6 h. An increase in PGE2 concentration occurs in brain cortex after 2-6 h of the onset of stress as well as an enhancement of COX-2 protein.	Dinoprostone	146-150	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	252-257	
12773326-7	2003	IH-induced COX-2 upregulation was associated with increased PGE2 tissue levels, neuronal apoptosis, and neurobehavioral deficits.	Dinoprostone	60-64	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	11-16	
12876297-11	2003	Based on these data, we conclude that 11,12-EET suppresses generation of PGE2 in monocytes via modulating the activity of COX-2.	Dinoprostone	73-77	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	122-127	
14581763-11	2003	Expression of COX-2 was up-regulated in the stomach as early as 2 h after 2DG treatment, and the PGE2 content was increased when determined 6 h later, in a COX-2-dependent/rofecoxib-sensitive manner.	Dinoprostone	97-101	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	156-161	
12576462-3	2003	EXPERIMENTAL DESIGN: The expression of COX-2 in primary microglia cultures obtained from intracranial rat C6 gliomas was examined using reverse transcription-PCR, Western analysis, and prostaglandin E(2) (PGE(2)) enzyme immunoassay.	Dinoprostone	185-203	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	39-44	
14592548-6	2003	Recruitment of COX-2 is initiated in the renal cortex and proceeds to the medulla associated with: (1) COX-2 mRNA accumulation; (2) increased COX-2 expression; and (3) a two-fold increase in PGE2 production by cortical microsomes.	Dinoprostone	191-195	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	15-20	
12672535-6	2003	These data suggest that COX-2 is responsible for PAF-mediated PGE(2) release in primary astrocytes.	Dinoprostone	62-68	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	24-29	
12660439-17	2003	Such suppressions were ameliorated with COX-2 inhibitor suggesting a role for PGE2 in the suppressed T-cell-mediated immune function in neonatal sepsis.	Dinoprostone	78-82	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	40-45	
12120893-4	2002	RESULTS: The ulcer onset, characterized by up-regulation of NOS-2 and COX-2 protein expression, was reflected in a marked increase in the mucosal PGE2 generation and NOS-2 activity, whereas healing was accompanied by a drop in PGE2 and NOS-2 activity, and a decrease in COX-2 and NOS-2 protein expression.	Dinoprostone	146-150	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	70-75	
12438549-8	2002	We conclude that inhibition of COX-1, despite causing intestinal hypermotility, bacterial invasion, and iNOS expression, up-regulates the expression of COX-2, and the PGE2 produced by COX-2 counteracts deleterious events, and maintains the mucosal integrity.	Dinoprostone	167-171	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	152-157	
12438549-8	2002	We conclude that inhibition of COX-1, despite causing intestinal hypermotility, bacterial invasion, and iNOS expression, up-regulates the expression of COX-2, and the PGE2 produced by COX-2 counteracts deleterious events, and maintains the mucosal integrity.	Dinoprostone	167-171	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	184-189	
12438555-11	2002	A specific COX-2 inhibitor blocked the lansoprazole-induced increase in mucosal PGE2 and mucosal protection.	Dinoprostone	80-84	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	11-16	
12431747-1	2002	It has been proposed that prostaglandin (PG)E(2) production via a process catalyzed by the inducible isoform of cyclooxygenase (COX)-2 and activation of specific PGE(2) receptor subtypes within the preoptic/anterior hypothalamus (AH/POA) is the last step and unique pathway in the induction of a fever.	Dinoprostone	26-48	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	112-134	
12392817-5	2002	However, the activities of isolated COX-1 and COX-2 were inhibited by taiwanin C (IC(50)=1.06 and 9.31 microM, respectively), reflecting the inhibition of both COX-1- and COX-2-dependent PGE(2) production in the cell culture system.	Dinoprostone	187-193	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	46-51	
12438520-3	2002	In anesthetized rats treated with bacterial lipopolysaccharide (LPS) to induce the expression of COX-2, the marked increase in PGE2 production that followed bolus intravenous injection of arachidonic acid (3 mg x kg(-1)) was strongly inhibited by diclofenac but largely unaffected by the COX-2-selective inhibitor DFP (5,5- dimethyl-3-(2-propoxy)-4-methanesulfonylphenyl)-2(5H)-furanone).	Dinoprostone	127-131	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	97-102	
12438520-7	2002	These data show that when exposed to an inflammatory stimulus, rat whole blood produces increased levels of PGE2 through induction of COX-2 in blood leukocytes.	Dinoprostone	108-112	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	134-139	
12098671-1	2002	It was previously reported that the expression of cyclo-oxigenase-2 (COX-2) is induced by prostaglandin E(2) (PGE(2)) in vitro in an osteogenic cell line and organ culture, suggesting an autoamplification mechanism.	Dinoprostone	90-108	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	69-74	
12120893-4	2002	RESULTS: The ulcer onset, characterized by up-regulation of NOS-2 and COX-2 protein expression, was reflected in a marked increase in the mucosal PGE2 generation and NOS-2 activity, whereas healing was accompanied by a drop in PGE2 and NOS-2 activity, and a decrease in COX-2 and NOS-2 protein expression.	Dinoprostone	227-231	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	70-75	
11578113-6	2001	Western-blot analysis revealed that the induction of COX-2 protein by TPA was inhibited by compound 9 in parallel with the inhibition of PGE2 production.	Dinoprostone	137-141	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	53-58	
11804951-10	2002	The drastic DNA fragmentation induced by COX-2 inhibitor could be reversed completely by PGD2 and partially by PGE2.	Dinoprostone	111-115	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	41-46	
11564815-9	2001	Despite absent COX-2 protein, SC-236, a putative COX-2-specific inhibitor, decreased mPGES RNA expression and PGE(2) concentration.	Dinoprostone	110-116	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	49-54	
11578113-8	2001	These findings suggest that 4"-methoxyl and 6"-methoxyl groups are required for the expression of more potent inhibitory activity against PGE2 production, and that the inhibition of PGE2 production by these 2"-hydroxychalcone derivatives is due to the inhibition of TPA-induced COX-2 protein expression.	Dinoprostone	182-186	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	278-283	
11356914-13	2001	Therefore, PGE(2) produced by COX-2 seems to be responsible for the profuse fluid secretion induced by CT, and COX-2 appears to be a specific target for the treatment of Asiatic cholera.	Dinoprostone	11-17	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	30-35	
11192947-11	2000	Indomethacin and both COX-2 inhibitors significantly prolonged the ulcer healing, while suppressing the generation of PGE2 in non-ulcerated and ulcerated gastric mucosa and the GBF at ulcer margin.	Dinoprostone	118-122	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	22-27	
11286400-8	2001	These results suggest that FR188582, a highly selective COX-2 inhibitor, has a potent anti-inflammatory effect mediated by inhibition of PGE2 in inflamed tissues.	Dinoprostone	137-141	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	56-61	
11549833-14	2001	Indomethacin and both COX-2 inhibitors significantly prolonged ulcer healing, while suppressing the generation of PGE2 in non-ulcerated and ulcerated gastric mucosa and GBF at the ulcer margin.	Dinoprostone	114-118	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	22-27	
10864144-9	2000	FR140423 has a potent anti-inflammatory effect mediated by inhibition of PGE2 produced by COX-2 in inflamed tissues.	Dinoprostone	73-77	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	90-95	
10963468-8	2000	Anti-inflammatory diets, including nutraceutical applications of CLA, may be beneficial in moderating cyclooygenase 2 (COX-2) activity or expression (influencing PGE2 biosynthesis) and might help to reduce rheumatoid arthritis (secondary osteoporosis).	Dinoprostone	162-166	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	119-124	
10854230-5	2000	Compared with control, complement-treated GEC produced 32% more prostaglandin (PG) E(2) in the presence of exogenous substrate, and the increase was abolished with the COX-2-selective inhibitor, NS-398.	Dinoprostone	64-87	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	168-173	
10102698-9	1999	Hyperglycemia/diabetes-induced downregulation of embryonic COX-2 gene expression may be a primary event in diabetic embryopathy, leading to lowered PGE2 levels and dysmorphogenesis.	Dinoprostone	148-152	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	59-64	
10807497-7	2000	Both selective COX-2 inhibitor and cPLA2 inhibitor abolished PGE2 generation, whereas an sPLA2 inhibitor partially inhibited it.	Dinoprostone	61-65	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	15-20	
11193597-3	2000	The selective COX-2 inhibitors NS-398 and DFU completely suppressed cholera toxin-induced prostaglandin E2 biosynthesis and caused a dose-dependent inhibition of cholera toxin-induced fluid secretion in the rat jejunum in vivo.	Dinoprostone	90-106	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	14-19	
10660836-3	2000	ROFA treatment induced a marked increase in the level of prostagladin E2 (PGE2) recovered in the bronchoalveolar lavage fluid (BALF), which was effectively decreased by pretreating the animals with the specific COX2 inhibitor NS398.	Dinoprostone	74-78	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	211-215	
10461889-7	1999	Indomethacin and NS398, a selective COX2 inhibitor, comparably decreased both the basal and the ET-stimulated PGE2 production.	Dinoprostone	110-114	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	36-40	
10461889-11	1999	The present study shows that ET is an inducer of astrocytic COX2 and suggests that ET-induced PGE2 production through COX2 may be involved in the regulation of astrocytic functions.	Dinoprostone	94-98	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	60-64	
10461889-11	1999	The present study shows that ET is an inducer of astrocytic COX2 and suggests that ET-induced PGE2 production through COX2 may be involved in the regulation of astrocytic functions.	Dinoprostone	94-98	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	118-122	
10723268-5	2000	Therefore, it was suggested that auranofin inhibited PGE2 production by inhibiting the COX-2 protein induction in TPA-stimulated macrophages.	Dinoprostone	53-57	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	87-92	
10366782-5	1999	Western blot analysis revealed that the induction of COX-2 by TPA or thapsigargin was inhibited by the two compounds in parallel with the inhibition of prostaglandin E2 production.	Dinoprostone	152-168	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	53-58	
10371510-5	1999	In this model, COX 2 protein expression peaked initially at 2 hours, associated with maximal prostaglandin E2 synthesis.	Dinoprostone	93-109	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	15-20	
10231640-1	1999	PURPOSE: Cyclooxygenase, either the cox1 or cox2 isoform, controls synthesis of prostaglandin E2 (PGE2), which regulates expression of matrix metalloprotease-9 (MMP-9).	Dinoprostone	80-96	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	44-48	
10231640-1	1999	PURPOSE: Cyclooxygenase, either the cox1 or cox2 isoform, controls synthesis of prostaglandin E2 (PGE2), which regulates expression of matrix metalloprotease-9 (MMP-9).	Dinoprostone	98-102	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	44-48	
10231640-16	1999	CONCLUSION: Indomethacin attenuates aneurysm growth, and its effects are mediated via inhibition of the cox2 isoform of cyclooxygenase, which decreases PGE2 and MMP-9 synthesis.	Dinoprostone	152-156	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	104-108	
10030841-6	1999	Pretreatment of cells with indomethacin or the COX-2 specific inhibitor NS-398 attenuated the suppressive effect of exogenous PGE2 on PDGF-Ralpha, indicating that endogenous PGE2 released by IL-1beta treatment also contributed to downregulation of PDGF-Ralpha.	Dinoprostone	126-130	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	47-52	
10030841-6	1999	Pretreatment of cells with indomethacin or the COX-2 specific inhibitor NS-398 attenuated the suppressive effect of exogenous PGE2 on PDGF-Ralpha, indicating that endogenous PGE2 released by IL-1beta treatment also contributed to downregulation of PDGF-Ralpha.	Dinoprostone	174-178	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	47-52	
9831332-1	1998	Cyclooxygenase (COX)-2 was induced in an acute exudative inflammatory model (rat carrageenin-induced pleurisy) in which prostaglandin E2, 6-keto-prostaglandin F1alpha, and thromboxane B2 were generated in the pleural fluid.	Dinoprostone	120-136	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	0-22	
10667306-5	1999	The induced immediate response is often mediated by COX-2 rather than by COX-1, especially when the end product is PGE2.	Dinoprostone	115-119	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	52-57	
9893949-7	1998	In the latter, the inducibility of COX-2 increased with time in culture, paralleling the acquisition of a more "activated" microglial phenotype, and appeared to account for the time-dependent increase in the PGE2/TXB2 production ratio.	Dinoprostone	208-212	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	35-40	
9893949-9	1998	On the other hand, COX-2 expression was up-regulated by the macrophage-deactivating cytokine TGF-beta 1, by exogenous PGE2 itself, which acted through EP2 receptors linked to cyclic AMP generation, and by non steroidal anti-inflammatory drugs.	Dinoprostone	118-122	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	19-24	
9831332-2	1998	Selective COX-2 inhibitors, such as NS-398, inhibited the plasma exudation and generation of prostaglandin E2, but not that of thromboxane B2 and 6-keto-prostaglandin F1alpha, in the pleural fluid.	Dinoprostone	93-109	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	10-15	
10189073-7	1998	In LPS-treated rats, the production of PGE2 was significantly higher than in the lungs of control rats, probably due to the induction of COX-2.	Dinoprostone	39-43	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	137-142	
9765332-14	1998	These findings demonstrate that 1) in normal bladders, the activation of B1 and B2 receptors evokes contraction that is largely mediated by COX-1 metabolites, whereas the COX-2 appears to be involved in PGE2 production after the activation of B1 receptor only, without interfering with contraction, and 2) in inflamed bladders, the activation of B1 and B2 receptors still produce PGE2, but the contractile response is not reduced by COX inhibitors, a result that indicates that additional mechanisms play a compensatory role.	Dinoprostone	203-207	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	171-176	
9765332-14	1998	These findings demonstrate that 1) in normal bladders, the activation of B1 and B2 receptors evokes contraction that is largely mediated by COX-1 metabolites, whereas the COX-2 appears to be involved in PGE2 production after the activation of B1 receptor only, without interfering with contraction, and 2) in inflamed bladders, the activation of B1 and B2 receptors still produce PGE2, but the contractile response is not reduced by COX inhibitors, a result that indicates that additional mechanisms play a compensatory role.	Dinoprostone	380-384	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	171-176	
9681442-8	1998	Furthermore, TGFbeta1 enhanced COX activity; the inhibitor indomethacin completely blocked TGFbeta1-mediated PGE2 synthesis.	Dinoprostone	109-113	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	31-34	
9681442-14	1998	Thus, TGFbeta1-induced increases in PGE2 concentration are regulated by COX.	Dinoprostone	36-40	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	72-75	
10189073-9	1998	LC at higher concentrations (6.8 x 10(-5) M) and INDO 10(-6) M inhibited PGE2 formed by COX-2 and also partly by COX-1 activity.	Dinoprostone	73-77	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	88-93	
9635881-7	1998	Transcripts of the inducible COX-2 gene were not detectable in the menhaden oil groups, but this gene was expressed in animals fed either level of safflower oil and in the HFS group was associated with increased levels of COX enzymatic activity and production of PGE2.	Dinoprostone	263-267	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	29-34	
9152412-5	1997	The COX-2 inhibitors NS-398 and nimesulide only slightly inhibited PGE2 production, whereas the COX-1/COX-2 inhibitors indomethacin, piroxicam and tenoxicam strongly inhibited PGE2 production.	Dinoprostone	67-71	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	4-9	
9568691-8	1998	In an analogous manner, TLCK (100 micromol/l) and MG 132 (10 micromol/l) inhibited IL-1beta-induced COX-2 enzyme activity (PGE2 formation) and COX-2 gene expression at the level of mRNA and protein.	Dinoprostone	123-127	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	100-105	
9152412-12	1997	We found that auranofin stimulated COX-1-dependent PGE2 production but inhibited COX-2-dependent PGE2 production in a concentration-dependent manner.	Dinoprostone	97-101	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	81-86	
9510202-3	1998	Cells treated with LPS predominantly produced PGE2 during culture for 3 to 24 h (delayed response), where cPLA2 and secretory PLA2 functioned cooperatively with inducible COX-2, which was, in turn, coupled with inducible PGE2 synthase.	Dinoprostone	46-50	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	171-176	
9430720-4	1998	Delayed PGE2 generation was also suppressed markedly by the cPLA2 inhibitor arachidonoyl trifluoromethyl ketone (AACOCF3), which attenuated induction of type IIA sPLA2, but not COX-2, expression.	Dinoprostone	8-12	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	177-182	
9663836-10	1997	Pre-treatment with prostaglandin E2 prevented the induction of COX-2 by aspirin.	Dinoprostone	19-35	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	63-68	
9152412-5	1997	The COX-2 inhibitors NS-398 and nimesulide only slightly inhibited PGE2 production, whereas the COX-1/COX-2 inhibitors indomethacin, piroxicam and tenoxicam strongly inhibited PGE2 production.	Dinoprostone	176-180	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	102-107	
9152412-9	1997	In this case, both the COX-2 and the COX-1/ COX-2 inhibitors inhibited PGE2 production.	Dinoprostone	71-75	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	23-28	
9152412-9	1997	In this case, both the COX-2 and the COX-1/ COX-2 inhibitors inhibited PGE2 production.	Dinoprostone	71-75	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	44-49	
9152412-10	1997	This suggest that under these conditions, PGE2 production is dependent on COX-2.	Dinoprostone	42-46	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	74-79	
8647962-7	1996	Therapeutic administration of a selective COX-2 inhibitor, SC-58125, rapidly reversed paw edema and reduced the level of PGE2 in paw tissue to baseline.	Dinoprostone	121-125	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	42-47	
9020023-3	1997	Pharmacological studies showed that formation of PGE2 was mediated predominantly by COX-2, PGD2 by COX-1, and TXB2 by both COX-1 and COX-2 depending upon the timing of LPS stimulation.	Dinoprostone	49-53	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	84-89	
9020023-3	1997	Pharmacological studies showed that formation of PGE2 was mediated predominantly by COX-2, PGD2 by COX-1, and TXB2 by both COX-1 and COX-2 depending upon the timing of LPS stimulation.	Dinoprostone	49-53	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	133-138	
9020023-5	1997	Thus, concordant induction of terminal PGE2 synthase with COX-2 leads to the preferred production of PGE2 to TXB2 and PGD2 by LPS-stimulated macrophages.	Dinoprostone	39-43	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	58-63	
8913778-2	1996	The selective adenosine A2a-receptor agonist CGS21680 and the non-selective adenosine A1- and A2-receptor agonist 5"-N-ethylcarboxiamidoadenosine (NECA) induced an increase in COX-2 mRNA levels and the synthesis of prostaglandin E2 (PGE2).	Dinoprostone	215-231	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	176-181	
8913778-2	1996	The selective adenosine A2a-receptor agonist CGS21680 and the non-selective adenosine A1- and A2-receptor agonist 5"-N-ethylcarboxiamidoadenosine (NECA) induced an increase in COX-2 mRNA levels and the synthesis of prostaglandin E2 (PGE2).	Dinoprostone	233-237	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	176-181	
7492303-5	1995	Hyperosmotic stimulation of PGE2 production was accompanied by a strong induction of Cox-2 mRNA levels and an increase in immunoreactive Cox-2, whereas the levels of immunoreactive phospholipase A2 and cyclooxygenase-1 did not change significantly.	Dinoprostone	28-32	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	85-90	
7492303-5	1995	Hyperosmotic stimulation of PGE2 production was accompanied by a strong induction of Cox-2 mRNA levels and an increase in immunoreactive Cox-2, whereas the levels of immunoreactive phospholipase A2 and cyclooxygenase-1 did not change significantly.	Dinoprostone	28-32	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	137-142	
7492303-6	1995	Dexamethasone, indomethacin and the selective Cox-2 inhibitor, NS-398, abolished the hypertonicity-induced stimulation of PGE2 formation; dexamethasone also prevented the increase in Cox-2 mRNA and protein.	Dinoprostone	122-126	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	46-51	
7492303-6	1995	Dexamethasone, indomethacin and the selective Cox-2 inhibitor, NS-398, abolished the hypertonicity-induced stimulation of PGE2 formation; dexamethasone also prevented the increase in Cox-2 mRNA and protein.	Dinoprostone	122-126	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	183-188	
7759893-8	1995	Two relatively selective inhibitors of COX-2 abolished the PAF-dependent increase in PGE2 production.	Dinoprostone	85-89	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	39-44	
34610503-9	2021	These results indicate that PGE2 increases COX-2 protein in microglia through the EP2 receptor supporting the idea that extracellular PGE2 has a triggering aspect for microglial activation.	Dinoprostone	28-32	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	43-48	
7637265-4	1995	The dose dependent effect of genistein on inhibition of mRNA for COX II correlated with the inhibition of the release of PGE2 into the media.	Dinoprostone	121-125	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	65-71	
7532080-6	1994	COX activity was assessed by the generation of prostacyclin (PGI2, measured as the stable metabolite, 6-keto prostaglandin F1 alpha) and prostaglandin E2 (PGE2).	Dinoprostone	137-153	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	0-3	
7532080-6	1994	COX activity was assessed by the generation of prostacyclin (PGI2, measured as the stable metabolite, 6-keto prostaglandin F1 alpha) and prostaglandin E2 (PGE2).	Dinoprostone	155-159	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	0-3	
34610503-3	2021	In the present study, we report that PGE2 increases COX-2 protein in microglia.	Dinoprostone	37-41	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	52-57	
34610503-4	2021	In a culture system, PGE2 at 10-6 M for 3 h increased COX-2 and microsomal PGE synthase (mPGES)-1 mRNA levels, and reduced mPGES-2, but did not affect COX-1 or cytosolic PGE synthase (cPGES) in microglia.	Dinoprostone	21-25	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	54-59	
34610503-5	2021	PGE2 at 10-6 M for 3 h also increased the COX-2 protein level, but did not affect COX-1, mPGES-1, mPGES-2, or cPGES.	Dinoprostone	0-4	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	42-47	
34610503-7	2021	Similar to PGE2, ONO-AE1-259-01 increased the COX-2 protein level, but did not affect COX-1, mPGES-1, mPGES-2, or cPGES.	Dinoprostone	11-15	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	46-51	
34610503-9	2021	These results indicate that PGE2 increases COX-2 protein in microglia through the EP2 receptor supporting the idea that extracellular PGE2 has a triggering aspect for microglial activation.	Dinoprostone	134-138	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	43-48	
32928206-9	2020	YHQ treatment also reversed the increased level of PGE2 through down-regulation of COX-2.	Dinoprostone	51-55	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	83-88	
34116703-0	2021	D-dopachrome tautomerase activates COX2/PGE2 pathway of astrocytes to mediate inflammation following spinal cord injury.	Dinoprostone	40-44	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	35-39	
34116703-9	2021	D-DT was able to activate the COX2/PGE2 signal pathway of astrocytes through CD74 receptor, and the intracellular activation of mitogen-activated protein kinases (MAPKs) was involved in the regulation of D-DT action.	Dinoprostone	35-39	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	30-34	
34998360-12	2022	In conclusion, TPRG1 promoted inflammation and cell proliferation of cystitis glandularis through activation of NF-kB/COX2/PGE2 axis.	Dinoprostone	123-127	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	118-122	
33155431-7	2021	Downregulation of miR-34a-5p inhibited the expression of IL-1beta/COX2/PGE2, decreased IL-1beta, PGE2 and CGRP release and upregulated the expression of SIRT1 in trigeminal ganglion, while overexpression of miR-34a-5p enhanced the expression of IL-1beta/COX2/PGE2, increased the release of IL-1beta, PGE2 and CGRP, and decreased the expression of SIRT1 in trigeminal ganglion.	Dinoprostone	71-75	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	66-70	
33155431-9	2021	In summary, these findings suggest that miR-34a-5p up-regulates the IL-1beta/COX2/PGE2 inflammation pathway, induces apoptosis, and enhances release of CGRP via inhibition of SIRT1 expression in trigeminal ganglion neurons, and thus miR-34a-5p may have potential as a therapeutic target for treatment of migraine.	Dinoprostone	82-86	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	77-81	
33147823-6	2020	Furthermore, all tested flavones inhibited the expression of iNOS and COX-2, which resulted in suppressing inflammatory cytokines including TNF-alpha, NO, and PGE2.	Dinoprostone	159-163	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	70-75	
32621176-7	2021	In this study, qRT-PCR and immunoblotting demonstrated that the key enzymes in PGE2 synthesis, including COX-1, COX-2, mPGES-1 and mPGES-2, were upregulated during cerebral I/R injury, but 15-PGDH, the main PGE2 degradation enzyme, was downregulated.	Dinoprostone	79-83	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	112-117	
31490357-4	2020	In this study, we evaluate the effect of blockade of the low affinity pro-inflammatory receptors EP1 and EP2 on expression of COX-2, the rate limiting enzyme in PGE2 biosynthesis, and on gut barrier permeability using cultured enterocytes and three different models of intestinal injury.	Dinoprostone	161-165	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	126-131	
31490357-5	2020	PGE2 upregulated COX-2 in IEC-6 enterocytes, and this response was blocked by the EP2 antagonist PF-04418948, but not by the EP1 antagonist ONO-8711 or EP4 antagonist E7046.	Dinoprostone	0-4	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	17-22	
31490357-8	2020	Our results indicate that the EP2 receptor plays a critical role in the positive feedback regulation of intestinal COX-2 by its end-product PGE2 during inflammation and may be a novel therapeutic target in the treatment of NEC.	Dinoprostone	140-144	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	115-120	
32165825-14	2020	Conclusions: These results indicate that the COX-2/PGE2/EPs pathway is involved in retinal damage and astrocyte inflammation.	Dinoprostone	51-55	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	45-50	
32290032-8	2020	Our results further showed that pretreatment with gold clusters dramatically inhibited the LPS-stimulated transcription and expression of COX2 and iNOS, and the subsequent prostaglandin E2 (PGE2) and nitric oxide (NO) production in HBZY-1 cells.	Dinoprostone	172-188	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	138-142	
32290032-8	2020	Our results further showed that pretreatment with gold clusters dramatically inhibited the LPS-stimulated transcription and expression of COX2 and iNOS, and the subsequent prostaglandin E2 (PGE2) and nitric oxide (NO) production in HBZY-1 cells.	Dinoprostone	190-194	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	138-142	
32361295-5	2020	qRT-PCR analysis and determination of PGE2 and LTB4 in the rat paw tissues indicated that this thiazole based dual inhibitor significantly reduced the expression of COX-2 and 5-LOX genes besides the marked reduction in both PGE2 and LTB4 levels.	Dinoprostone	38-42	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	165-176	
31539536-2	2019	We previously reported that cyclo-oxygenase (COX)-2, a rate-limiting enzyme for prostaglandin E2 (PGE2) synthesis, significantly enhanced depressive-like disorders induced by chronic stress in rats.	Dinoprostone	80-96	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	28-51	
31797003-8	2020	CONCLUSIONS: Acute changes in colonic mucosa PGE2 provided a rapid means of predicting long-term chemopreventive effects from celecoxib, and might be useful for screening of new COX-2 inhibitor compounds.	Dinoprostone	45-49	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	178-183	
31565858-0	2019	Sodium butyrate attenuates angiotensin II-induced cardiac hypertrophy by inhibiting COX2/PGE2 pathway via a HDAC5/HDAC6-dependent mechanism.	Dinoprostone	89-93	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	84-88	
31565858-8	2019	Mechanistically, NaBu inhibited the expression of COX2/PGE2 along with production of ANP and phosphorylated ERK (pERK) stimulated by Ang II in in vivo and in vitro, which was accompanied by the suppression of HDAC5 and HDAC6 activities.	Dinoprostone	55-59	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	50-54	
31565858-9	2019	Additionally, knocking down the expression of HDAC5 and HDAC6 via gene-editing strategy dramatically blocked Ang II-induced hypertrophic responses through COX2/PGE2 pathway.	Dinoprostone	160-164	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	155-159	
31565858-10	2019	These results provide solid evidence that NaBu attenuates Ang II-induced cardiac hypertrophy by inhibiting the activation of COX2/PGE2 pathway in a HDAC5/HDAC6-dependent manner.	Dinoprostone	130-134	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	125-129	
31539536-2	2019	We previously reported that cyclo-oxygenase (COX)-2, a rate-limiting enzyme for prostaglandin E2 (PGE2) synthesis, significantly enhanced depressive-like disorders induced by chronic stress in rats.	Dinoprostone	98-102	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	28-51	
31320912-14	2019	Moreover, compared with the control group, the protein and gene expression of COX-2, HIF-1alpha, VEGFR1, and VEGFR2 in gastric tissues of pylorus was obviously increased and the serum PGE2 level was significantly deceased in CAG rats, which could be significantly counteracted by WQD administration.	Dinoprostone	184-188	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	78-83	
31306980-8	2019	Furthermore, COX-2 inhibitors significantly reduced prostaglandin E2 production.	Dinoprostone	52-68	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	13-18	
31382970-11	2019	Interestingly, this in vitro study revealed that the MSCs pretreated with a COX-2 inhibitor had little effect on M2 macrophage polarization, but this phenomenon could be reversed by adding prostaglandin E2 (PGE2).	Dinoprostone	189-205	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	76-81	
31382970-11	2019	Interestingly, this in vitro study revealed that the MSCs pretreated with a COX-2 inhibitor had little effect on M2 macrophage polarization, but this phenomenon could be reversed by adding prostaglandin E2 (PGE2).	Dinoprostone	207-211	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	76-81	
31382970-13	2019	The underlying mechanisms may include MSC-enhanced M2 macrophage polarization via the COX-2-PGE2 pathway.	Dinoprostone	92-96	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	86-91	
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.	Dinoprostone	113-117	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	0-5	
30981278-11	2019	Astrocytes responded robustly to the MIF interference, by which regulated MAPK/COX2/PGE2 signal pathway through coupling with the CD74 membrane receptor.	Dinoprostone	84-88	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	79-83	
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.	Dinoprostone	39-43	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	29-34	
30733814-8	2019	Conclusions: The purgative property of the purified resin glycoside fraction was attributed to NF-kappaB activation in the colon, which increased the COX-2-mediated secretion of PGE2.	Dinoprostone	178-182	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	150-155	
30526621-9	2018	RESULTS: The expression of cyclo-oxygenase (COX)-2, which is responsible for production of the pro-inflammatory factor PGE2 and thus glial activation, was increased in the CA1 hippocampus in a rat model of depression.	Dinoprostone	119-123	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	27-50	
30526621-12	2018	These effects were accompanied by an enhanced activity of the COX-2/PGE2 pathway and effectively induced core symptoms of depression.	Dinoprostone	68-72	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	62-67	
30618728-10	2018	Crocetin inhibited the COX-2 catalyzed prostaglandin (PGE2) and inducible nitric oxide synthase catalyzed NO production on RAW 264.7.	Dinoprostone	54-58	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	23-28	
30453998-8	2018	The inhibition of LPS-induced PGE2 release by the most potent candidate KIT 17 was partially dependent on reduced protein synthesis of mPGES-1 and COX-2.	Dinoprostone	30-34	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	147-152	
30098279-13	2018	The result of our present findings suggest that hesperidin may be a promising modulator in preventing renal cancer possibly by virtue of its ability to alleviate oxidative stress and inhibit COX-2/PGE2 pathway.	Dinoprostone	197-201	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	191-196	
29032204-8	2017	Preincubation of submucosa/mucosa preparations with Ang II for 10 min significantly increased PGE2 production, which was abolished by either COX-1 or COX-2 inhibitor.	Dinoprostone	94-98	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	150-155	
29204817-14	2018	As evident COX-2 catalyzes the synthesis of PGE2, needed in the activation of Wnt/beta-catenin pathway, which in turn is responsible for activating the transcriptional proteins required for higher degree of cell division and thence growth.	Dinoprostone	44-48	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	11-16	
29482802-10	2018	Hence, interaction with COX-2, NPY may affect the levels of PGF2alpha and PGE2 as well as impact the proliferation of granulosa cells in ovaries, thus further reducing the luteal formation, and promoting luteal structural and functional regression, as well as the ovarian steroidogenesis following EA treatment.	Dinoprostone	74-78	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	24-29	
29433672-15	2018	Meanwhile, beta-PAE increased cyclooxygenase enzyme activities (COX-1 and COX-2) to enhance the production of prostaglandin E2.	Dinoprostone	110-126	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	74-79	
28797762-5	2017	These findings show that ceramide enhances PE-induced vascular smooth muscle constriction by mediation of the ER stress/COX-2/PGE2 pathway.	Dinoprostone	126-130	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	120-125	
28765972-8	2017	YNB Inhibited the production of the COX-2 AA metabolite prostaglandin E2 (PGE2) and suppressed expression of COX-2, cPLA2, PGE2 mRNA in the carrageenan-induced inflammation mode (P<0.05).	Dinoprostone	56-72	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	36-41	
28765972-8	2017	YNB Inhibited the production of the COX-2 AA metabolite prostaglandin E2 (PGE2) and suppressed expression of COX-2, cPLA2, PGE2 mRNA in the carrageenan-induced inflammation mode (P<0.05).	Dinoprostone	74-78	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	36-41	
28642034-6	2017	RESULTS: The COX-2/PGE2 signaling pathway was activated in CBDL rat lung in vivo and PMVECs in vitro, which was due to the activation of NF-kappaB P65.	Dinoprostone	19-23	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	13-18	
28642034-9	2017	The BMP-2/CV-2 imbalance is dependent on the COX-2/PGE2 signaling pathway, and thus the effects of this imbalance can be reversed by adminstration of Parecoxib.	Dinoprostone	51-55	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	45-50	
27847198-0	2016	Ginsenoside-Rb1 ameliorates lithium-induced nephrotoxicity and neurotoxicity: Differential regulation of COX-2/PGE2 pathway.	Dinoprostone	111-115	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	105-110	
28228071-11	2017	The expression of iNOS and COX-2 was up-regulated in the small intestine in a time-dependent manner after ischemia caused by stenosis of the SMA, with increases in the mucosal contents of NO and PGE2.	Dinoprostone	195-199	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	27-32	
28349234-9	2017	Moreover, TMJ inflammation-induced upregulation of Nav1.7 expression and PGE2 levels in the TG could be reversed by COX-2-selective inhibitor meloxicam given by oral gavage, and meanwhile, the hyperalgesia of inflamed TMJ was also mitigated.	Dinoprostone	73-77	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	116-121	
27847198-9	2016	Interestingly, Li+ had a differential effect on cyclooxygenase (COX)-2/prostaglandin E2 (PGE2) pathway, as it significantly increased COX-2 expression and PGE2 level in the kidney, while decreasing them in the brain compared to control.	Dinoprostone	71-87	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	48-70	
27847198-9	2016	Interestingly, Li+ had a differential effect on cyclooxygenase (COX)-2/prostaglandin E2 (PGE2) pathway, as it significantly increased COX-2 expression and PGE2 level in the kidney, while decreasing them in the brain compared to control.	Dinoprostone	89-93	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	48-70	
27847198-9	2016	Interestingly, Li+ had a differential effect on cyclooxygenase (COX)-2/prostaglandin E2 (PGE2) pathway, as it significantly increased COX-2 expression and PGE2 level in the kidney, while decreasing them in the brain compared to control.	Dinoprostone	89-93	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	134-139	
27847198-9	2016	Interestingly, Li+ had a differential effect on cyclooxygenase (COX)-2/prostaglandin E2 (PGE2) pathway, as it significantly increased COX-2 expression and PGE2 level in the kidney, while decreasing them in the brain compared to control.	Dinoprostone	155-159	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	48-70	
27847198-10	2016	On the other hand, administering GRb1 with Li+ suppressed COX-2/PGE2 pathway in both kidney and brain compared to Li+ alone.	Dinoprostone	64-68	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	58-63	
27847198-12	2016	Furthermore, COX-2/PGE2 pathway has a mechanistic role in the nephro- and neuro-protective effects of GRb1 against Li+-induced toxicity.	Dinoprostone	19-23	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	13-18	
27535007-7	2016	Basal release of COX-2-derived PGE2 was higher in coronary arteries from OZR where the selective agonist of EP4 receptors TCS 2519 evoked potent relaxations.	Dinoprostone	31-35	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	17-22	
27535007-10	2016	CONCLUSION AND IMPLICATIONS: COX-2 contributes to cardiac oxidative stress and to the endothelium-independent O2.- -mediated coronary vasoconstriction induced by H2 O2 in obesity, which is offset by the release of COX-2-derived endothelial PGE2 acting on EP4 vasodilator receptors.	Dinoprostone	240-244	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	29-34	
27058422-7	2016	In conclusion, we are the first to systemically demonstrate in both animal and cell models that metformin inhibits bladder cancer progression by inhibiting stem cell repopulation through the COX2/PGE2/STAT3 axis.	Dinoprostone	196-200	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	191-195	
26515683-6	2015	Activation of ERK/JNK, NF-kappaB and COX-2/PGE2 were detected in heat-treated cells, which were mimicked by knockdown, and reversed by overexpression of CFTR or VX-809, a reported CFTR mutation corrector.	Dinoprostone	43-47	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	37-42	
25989136-9	2015	IL-1beta increased COX-2 protein and PGE2 production in RMLMC.. PGE2 induced relaxations in RMLMC, comparable to h-IL-1beta.	Dinoprostone	64-68	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	19-24	
25063066-6	2014	The detection at the molecular level showed decreased Bcl-2 expression, increased Bax expression, upregulated expression of NF-kappaB and its downstream factor COX-2/PGE2.	Dinoprostone	166-170	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	160-165	
26159321-2	2015	We identified a COX-2-derived pulsatile PGE2 release triggered by OT in rat ileum mucosa.	Dinoprostone	40-44	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	16-21	
24607321-6	2014	LPS surprisingly produced a time-dependent decrease in COX-1 protein which likely facilitates the COX-2-dependent production of prostaglandin E2 and prostacyclin.	Dinoprostone	128-144	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	98-103	
25070591-8	2015	COX-2 and PGE2 exhibited near-normal levels (p > 0.05) at LASER 3 (COX-2: 176.9 +- 75.4 / PGE2: 297.2 +- 259.6) and LASER 7 (COX-2: 259.2 +- 190.4 / PGE2: 587.1 +- 409.7).	Dinoprostone	93-97	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	0-5	
25070591-8	2015	COX-2 and PGE2 exhibited near-normal levels (p > 0.05) at LASER 3 (COX-2: 176.9 +- 75.4 / PGE2: 297.2 +- 259.6) and LASER 7 (COX-2: 259.2 +- 190.4 / PGE2: 587.1 +- 409.7).	Dinoprostone	93-97	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	0-5	
25169427-7	2014	These results suggest that the dual delayed effect of kinins on PGE2 synthesis may be due to differential regulation of COX-2 and signaling molecules such as p42/p44 MAPKs.	Dinoprostone	64-68	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	120-125	
24085626-9	2014	Similar to the effect of RA, both NAC and NS-398 (COX-2 inhibitor) blocked CoCl2-induced COX-2 expression and PGE2 secretion.	Dinoprostone	110-114	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	50-55	
24085626-11	2014	Taken together, RA protects primary cultured rat hepatocytes against CoCl2-induced cell injury through inhibition of ROS-activated p38MAPK and COX-2/PGE2 pathway.	Dinoprostone	149-153	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	143-148	
24064301-7	2014	In addition, S1P/S1P2-dependent upregulation of COX-2 led to significantly elevated PGE2 levels, which were further potentiated in the presence of Ang II and IL-1beta.	Dinoprostone	84-88	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	48-53	
24064301-10	2014	Overall, our results demonstrate that extracellular S1P induces COX-2 expression via activation of S1P2 and subsequent Gi and p42/p44 MAPK-dependent signaling in renal mesangial cells leading to enhanced PGE2 formation and cell migration that essentially requires COX-2.	Dinoprostone	204-208	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	64-69	
23263903-6	2013	The activity of COX-2 (production of prostaglandin-E(2)) was also determined by high pressure liquid chromatography.	Dinoprostone	37-55	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	16-21