PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 22975359-9 2013 These data suggest that COX-2-derived vasodilator prostanoids, PGI2 and PGE2, produced during endotoxemia increase iNOS protein expression and activity as well as peroxynitrite formation resulting in decreased CYP4A1 protein expression and 20-HETE synthesis. Dinoprostone 72-76 nitric oxide synthase 2 Rattus norvegicus 115-119 22089194-4 2012 In LPS-treated microglia, paeonol attenuated the overexpression of inducible nitric oxide synthase and cyclooxygenase 2, leading to the decrease in nitric oxide and prostaglandin E2 production, respectively. Dinoprostone 165-181 nitric oxide synthase 2 Rattus norvegicus 67-98 14988416-8 2004 These results demonstrate that in the LPS-treated rat gastric mucosa, PGE2 enhances the release of NO after activation of iNOS, although NO produced by iNOS does not stimulate the release of PGE2 by COXs. Dinoprostone 70-74 nitric oxide synthase 2 Rattus norvegicus 122-126 19583997-5 2009 Parallel to the decreases in NO and PGE(2) production was a reduction in the expression of inducible NO synthase (iNOS) and cyclooxygenase 2 (COX-2) as measured by mRNA and protein levels. Dinoprostone 36-42 nitric oxide synthase 2 Rattus norvegicus 91-112 19583997-5 2009 Parallel to the decreases in NO and PGE(2) production was a reduction in the expression of inducible NO synthase (iNOS) and cyclooxygenase 2 (COX-2) as measured by mRNA and protein levels. Dinoprostone 36-42 nitric oxide synthase 2 Rattus norvegicus 114-118 19299804-7 2009 CONCLUSIONS: Based on these results, it is suggested that the inhibition of NO and prostaglandin E(2) over-production through suppressing iNOS and COX-2 induction and attenuation of TNF-alpha formation and neutrophil infiltration into inflammatory sites by C-PC may contribute, at least in part, to its antihyperalgesic activity. Dinoprostone 83-101 nitric oxide synthase 2 Rattus norvegicus 138-142 18216606-8 2008 MEASUREMENTS AND MAIN RESULTS: The nonselective COX inhibitors salicylate and indomethacin enhanced the expression of iNOS in the rat gastric mucosa and exacerbated gastric injury in the presence of lipopolysaccharide, effects reversed by exogenous prostaglandin E2. Dinoprostone 249-265 nitric oxide synthase 2 Rattus norvegicus 118-122 17091492-0 2007 TNF-alpha/IFN-gamma-induced iNOS expression increased by prostaglandin E2 in rat primary astrocytes via EP2-evoked cAMP/PKA and intracellular calcium signaling. Dinoprostone 57-73 nitric oxide synthase 2 Rattus norvegicus 28-32 17091492-4 2007 Pharmacological and RNA interference approaches further indicated the involvement of the receptor EP2 in PGE(2)-induced iNOS upregulation in T/I-treated astrocytes. Dinoprostone 105-111 nitric oxide synthase 2 Rattus norvegicus 120-124 17091492-5 2007 Quantitative real-time polymerase chain reaction and gel mobility shift assays also demonstrated that PGE(2) increased iNOS transcription through EP2-induced cAMP/protein kinase A (PKA)-dependent pathway. Dinoprostone 102-108 nitric oxide synthase 2 Rattus norvegicus 119-123 17067575-2 2007 Since surgical sympathectomy produces most of the retinal changes noted in the retina of an STZ-treated rat in a non-diabetic rat, we wanted to determine whether sympathetic neurotransmission regulates gene and protein expression of inducible nitric oxide synthase (iNOS) and the prostaglandin (PGE2) receptor, as well as the levels of PGE2. Dinoprostone 295-299 nitric oxide synthase 2 Rattus norvegicus 233-264 16170330-7 2005 Analysis of mRNA expression for iNOS, COX-2 and CINC-2 in lung tissue showed an upregulation of these enzymes, which paralleled elevated levels of LTB4, PGE2, TNF-alpha, IL-6 and NO2- in BAL fluid. Dinoprostone 153-157 nitric oxide synthase 2 Rattus norvegicus 32-36 15067210-5 2004 RESULTS: The present work shows that iNOS inhibitor, aminoguanidine, reduced NO and PGE(2)/PGF(2alpha) production induced by LPS injection. Dinoprostone 84-90 nitric oxide synthase 2 Rattus norvegicus 37-41 12794049-2 2003 iNOS activated cyclooxgenase, causing elevated prostaglandin E(2) (PGE(2)) and F(2 alpha) in the adrenals, but had no effect on lipoxygenase. Dinoprostone 47-65 nitric oxide synthase 2 Rattus norvegicus 0-4 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 nitric oxide synthase 2 Rattus norvegicus 60-65 12490607-2 2003 The purpose of the present study was to pharmacologically inhibit cyclooxygenase-2 (COX-2) and inducible NO synthase (iNOS) to 1) explore the prostaglandin contribution to blood-cerebrospinal fluid barrier permeability alterations and 2) elucidate the in vivo concentration relationship between prostaglandin E2 (PGE2) and NO during experimental meningitis. Dinoprostone 295-311 nitric oxide synthase 2 Rattus norvegicus 95-116 12490607-2 2003 The purpose of the present study was to pharmacologically inhibit cyclooxygenase-2 (COX-2) and inducible NO synthase (iNOS) to 1) explore the prostaglandin contribution to blood-cerebrospinal fluid barrier permeability alterations and 2) elucidate the in vivo concentration relationship between prostaglandin E2 (PGE2) and NO during experimental meningitis. Dinoprostone 295-311 nitric oxide synthase 2 Rattus norvegicus 118-122 12490607-2 2003 The purpose of the present study was to pharmacologically inhibit cyclooxygenase-2 (COX-2) and inducible NO synthase (iNOS) to 1) explore the prostaglandin contribution to blood-cerebrospinal fluid barrier permeability alterations and 2) elucidate the in vivo concentration relationship between prostaglandin E2 (PGE2) and NO during experimental meningitis. Dinoprostone 313-317 nitric oxide synthase 2 Rattus norvegicus 95-116 12490607-2 2003 The purpose of the present study was to pharmacologically inhibit cyclooxygenase-2 (COX-2) and inducible NO synthase (iNOS) to 1) explore the prostaglandin contribution to blood-cerebrospinal fluid barrier permeability alterations and 2) elucidate the in vivo concentration relationship between prostaglandin E2 (PGE2) and NO during experimental meningitis. Dinoprostone 313-317 nitric oxide synthase 2 Rattus norvegicus 118-122 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 nitric oxide synthase 2 Rattus norvegicus 104-108 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 nitric oxide synthase 2 Rattus norvegicus 60-65 11584082-10 2001 The PGE(2) increase was associated with NOS2-mediated activation of COX and induction of mPGES. Dinoprostone 4-10 nitric oxide synthase 2 Rattus norvegicus 40-44 11564815-8 2001 The LPS-induced increase in PGE(2) concentration was mediated by NOS2-derived NO-dependent activation of COX-1 pathway and by induction of mPGES. Dinoprostone 28-34 nitric oxide synthase 2 Rattus norvegicus 65-69 11930633-16 2001 However, it retards the ulcer healing by inhibiting PGE2 production in iNOS expression and activity in gastric mucosa. Dinoprostone 52-56 nitric oxide synthase 2 Rattus norvegicus 71-75 10213270-7 1999 The increase in iNOS activity in the colon was preceded by macroscopic inflammatory lesions, like hyperemia, ulcerations and edema formation as well as neutrophil accumulation in the gastric mucosa and increased circulating concentrations of PGE2 metabolite (PGEM). Dinoprostone 242-246 nitric oxide synthase 2 Rattus norvegicus 16-20 11334856-5 2001 Lipopolysaccharide increases prostaglandin E(2) synthesis by increasing cyclooxygenase-2 protein levels in rat bladder and prostaglandin E(2) synthesis may be further elevated by increases in nitric oxide caused by an up-regulation of inducible nitric oxide synthase (iNOS). Dinoprostone 123-141 nitric oxide synthase 2 Rattus norvegicus 268-272 11453100-10 2001 In addition the expression of cyclooxygenase-2 and inducible nitric oxide synthase proteins increased PGE2 generation and NOx secretion in the ulcerated stomach were suppressed by FR167653. Dinoprostone 102-106 nitric oxide synthase 2 Rattus norvegicus 51-82 10217523-8 1999 We have previously shown that bacterial endotoxin (LPS) strongly stimulates PGE2 and NO production in rat primary microglial cultures, by inducing the expression of the key enzymes cyclo-oxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS), respectively. Dinoprostone 76-80 nitric oxide synthase 2 Rattus norvegicus 211-242 9034831-0 1997 Inducible nitric oxide synthase expression in activated rat microglial cultures is downregulated by exogenous prostaglandin E2 and by cyclooxygenase inhibitors. Dinoprostone 110-126 nitric oxide synthase 2 Rattus norvegicus 0-31 9893949-10 1998 Interestingly, PGE2 utilized the same EP2 receptor-mediated signal transduction mechanism to down-regulate the expression of the inducible NO synthase and the production of NO. Dinoprostone 15-19 nitric oxide synthase 2 Rattus norvegicus 129-150 9724813-7 1998 The iNOS inhibitor aminoguanidine reduced PGE2 concentration in the infarct, where both iNOS and COX-2 were expressed, but not in the olfactory bulb, where only COX-2 was expressed. Dinoprostone 42-46 nitric oxide synthase 2 Rattus norvegicus 4-8 9034831-3 1997 In this study we show that exogenous prostaglandin E2 (PGE2), which is known to increase cyclic adenosine monophosphate (cAMP) levels in microglial cells, downregulates LPS-induced iNOS expression in a dose-dependent manner. Dinoprostone 37-53 nitric oxide synthase 2 Rattus norvegicus 181-185 9034831-3 1997 In this study we show that exogenous prostaglandin E2 (PGE2), which is known to increase cyclic adenosine monophosphate (cAMP) levels in microglial cells, downregulates LPS-induced iNOS expression in a dose-dependent manner. Dinoprostone 55-59 nitric oxide synthase 2 Rattus norvegicus 181-185 10200320-5 1999 Cyclopentenone prostaglandins were potent inhibitors of iNOS induction and were more effective than their precursors, prostaglandins E2 and D2. Dinoprostone 118-135 nitric oxide synthase 2 Rattus norvegicus 56-60 9034831-4 1997 The involvement of cAMP in the PGE2-dependent inhibition of iNOS is supported by several pieces of evidence. Dinoprostone 31-35 nitric oxide synthase 2 Rattus norvegicus 60-64 9034831-8 1997 Interestingly, the abrogation of endogenous prostanoid production by several COX inhibitors caused a reduction of iNOS expression, suggesting a positive modulatory effect of endogenous prostanoids of iNOS expression, as opposed to the inhibitory effect of exogenous PGE2. Dinoprostone 266-270 nitric oxide synthase 2 Rattus norvegicus 114-118 7527554-9 1994 These data suggest that (i) endogenous PGE2 downregulates iNOS induction, (ii) this inhibitory effect of PGE2 on iNOS induction is not mediated by activation of adenylate cyclase, and (iii) exogenous PGI2 stimulates COX induction possibly by activation of adenylate cyclase. Dinoprostone 39-43 nitric oxide synthase 2 Rattus norvegicus 58-62 7527554-9 1994 These data suggest that (i) endogenous PGE2 downregulates iNOS induction, (ii) this inhibitory effect of PGE2 on iNOS induction is not mediated by activation of adenylate cyclase, and (iii) exogenous PGI2 stimulates COX induction possibly by activation of adenylate cyclase. Dinoprostone 105-109 nitric oxide synthase 2 Rattus norvegicus 58-62 7527554-9 1994 These data suggest that (i) endogenous PGE2 downregulates iNOS induction, (ii) this inhibitory effect of PGE2 on iNOS induction is not mediated by activation of adenylate cyclase, and (iii) exogenous PGI2 stimulates COX induction possibly by activation of adenylate cyclase. Dinoprostone 105-109 nitric oxide synthase 2 Rattus norvegicus 113-117 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 nitric oxide synthase 2 Rattus norvegicus 61-65 33161252-1 2020 The development of NSAIDs/iNOS inhibitor hybrids is a new strategy for the treatment of inflammatory diseases by suppression of the overproduction of PGE2 and NO. Dinoprostone 150-154 nitric oxide synthase 2 Rattus norvegicus 26-30 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 nitric oxide synthase 2 Rattus norvegicus 147-151 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 nitric oxide synthase 2 Rattus norvegicus 147-151 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 nitric oxide synthase 2 Rattus norvegicus 18-22 32184716-6 2020 Hypothalamic COX-1 and -2, prostaglandin E synthase (PGES) and inducible nitric oxide synthase (iNOS) mRNA expression were all elevated in aged animals, leading to elevated PGE2 levels. Dinoprostone 173-177 nitric oxide synthase 2 Rattus norvegicus 63-94 30210652-5 2018 In order to detect the potential correlation between iNOS/NO expression, COX-2/PGE2 expression, and IVDD, we developed a P. acnes-induced IVDD rat model and found that the upregulation of iNOS/NO and COX-2/PGE2 was essential to the occurrence of P. acnes-induced IVDD. Dinoprostone 79-83 nitric oxide synthase 2 Rattus norvegicus 188-192 30210652-5 2018 In order to detect the potential correlation between iNOS/NO expression, COX-2/PGE2 expression, and IVDD, we developed a P. acnes-induced IVDD rat model and found that the upregulation of iNOS/NO and COX-2/PGE2 was essential to the occurrence of P. acnes-induced IVDD. Dinoprostone 206-210 nitric oxide synthase 2 Rattus norvegicus 188-192 27973680-4 2017 The potentiating effect of PGE2 was positively associated with increased expression of inducible nitric oxide synthase. Dinoprostone 27-31 nitric oxide synthase 2 Rattus norvegicus 87-118 25620059-7 2015 Genistein pre-treatment significantly inhibited the increased protein levels of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2), thereby reducing nitric oxide (NO) and prostaglandin-E2 (PGE) levels, respectively. Dinoprostone 188-204 nitric oxide synthase 2 Rattus norvegicus 80-111 24962643-6 2015 Moreover, LPS-induced expression of cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) was inhibited by ALA pretreatment, and consequently, the secretion levels of their respective enzymatic products prostaglandin E2 (PGE2) and nitric oxide (NO) were significantly decreased. Dinoprostone 217-233 nitric oxide synthase 2 Rattus norvegicus 65-96 24962643-6 2015 Moreover, LPS-induced expression of cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) was inhibited by ALA pretreatment, and consequently, the secretion levels of their respective enzymatic products prostaglandin E2 (PGE2) and nitric oxide (NO) were significantly decreased. Dinoprostone 217-233 nitric oxide synthase 2 Rattus norvegicus 98-102 24962643-6 2015 Moreover, LPS-induced expression of cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) was inhibited by ALA pretreatment, and consequently, the secretion levels of their respective enzymatic products prostaglandin E2 (PGE2) and nitric oxide (NO) were significantly decreased. Dinoprostone 235-239 nitric oxide synthase 2 Rattus norvegicus 65-96 24962643-6 2015 Moreover, LPS-induced expression of cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) was inhibited by ALA pretreatment, and consequently, the secretion levels of their respective enzymatic products prostaglandin E2 (PGE2) and nitric oxide (NO) were significantly decreased. Dinoprostone 235-239 nitric oxide synthase 2 Rattus norvegicus 98-102 25620059-7 2015 Genistein pre-treatment significantly inhibited the increased protein levels of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2), thereby reducing nitric oxide (NO) and prostaglandin-E2 (PGE) levels, respectively. Dinoprostone 188-204 nitric oxide synthase 2 Rattus norvegicus 113-117 25620059-7 2015 Genistein pre-treatment significantly inhibited the increased protein levels of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2), thereby reducing nitric oxide (NO) and prostaglandin-E2 (PGE) levels, respectively. Dinoprostone 206-209 nitric oxide synthase 2 Rattus norvegicus 80-111 25620059-7 2015 Genistein pre-treatment significantly inhibited the increased protein levels of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2), thereby reducing nitric oxide (NO) and prostaglandin-E2 (PGE) levels, respectively. Dinoprostone 206-209 nitric oxide synthase 2 Rattus norvegicus 113-117