ライフサイエンスコーパス: cyclooxygenase

1 n the biochemical response (lipoxygenase and cyclooxygenase).

2 ed activation of endothelial NO synthase and cyclooxygenase.

3 thrombin, the thrombospondin-1/CD36 axis and cyclooxygenase 1 in subsequent platelet activation and s

4 Similar to MSCs, ICC-SCs strongly expressed cyclooxygenase 1/2 and basally secreted prostaglandin E2

5 by aspirin in vitro or in vivo, implicating cyclooxygenase-1 (COX).

6 We developed a novel assay of cyclooxygenase-1 (COX-1) acetylation in platelets isolat

7 dal anti-inflammatory drugs (NSAIDs) inhibit cyclooxygenase-1 (COX-1) and COX-2 enzymes.

8 r studied in monoamine oxidase B (MAO-B) and cyclooxygenase-1 (COX-1) enzyme through molecular dockin

9 Deletion of cyclooxygenase-1 (Cox-1), an enzyme involved in producti

10 -nociceptors; for example, inhibition of the cyclooxygenase-1 (COX-1)-prostaglandin system within the

11 ction was also diminished in vessels lacking cyclooxygenase-1 [COX1 knockout (KO)] or the thromboxane

12 otal prostaglandin concentration and to show cyclooxygenase-1 and -2 (COX-1 and -2) immunoreactivitie

13 Cyclooxygenase-1 and -2 did not oxidize alkynyl linoleic

14 141.6 and 138.8 muM, respectively) inhibited cyclooxygenase-1 and -2 enzymes by 50%.

15 eries of uni-x sheep, accompanied by reduced cyclooxygenase-1 and -2 gene expression (P<0.05).

16 . canina hips showed some anti-inflammatory (cyclooxygenase-1 and 12-lipooxygense inhibition potency)

17 production of some monitored eicosanoids in cyclooxygenase-1 and 12-lipoxygenase pathways.

18 ilization [Ca(t)]i controls granule release, cyclooxygenase-1 and integrin activation, and phosphatid

19 spirin are consistent with the inhibition of cyclooxygenase-1 in platelets, we used liquid chromatogr

20 y supplied by PGE2, are removed secondary to cyclooxygenase-1 inhibition.

21 asal polyposis, and respiratory reactions to cyclooxygenase-1 inhibitors (nonsteroidal anti-inflammat

22 esults reveal 15(S)-HETE as a major platelet cyclooxygenase-1 product with strong proangiogenic effec

23 t effects through irreversible inhibition of cyclooxygenase-1, whereas its anticancer effects may be

24 here was no coexpression between mPGES-1 and cyclooxygenase-1.

25 tion of proangiogenic 15(S)-HETE by platelet cyclooxygenase-1.

26 ammatory targets of curcumin (i.e., mPGES-1, cyclooxygenases, 12/15-LOs, nuclear factor-kappaB, nucle

27 then examined their impact on expression of cyclooxygenase 2 (COX-2) and resultant prostaglandin E2

28 ed by detailed analysis of the regulation of cyclooxygenase 2 (COX-2) expression as a marker gene and

29 ted kinases (ERK) activity and the increased cyclooxygenase 2 (COX-2) expression as well as the mutag

30 creased proliferative capacity and a lowered cyclooxygenase 2 (Cox-2) expression in these organoids c

31 al MVECs, and CXCL8, CCL3, CCL4, VCAM-1, and cyclooxygenase 2 (COX-2) in cerebral MVECs.

32 result of increased expression of inducible cyclooxygenase 2 (COX-2) in placental tissues.

33 is occurs via TLR2-dependent upregulation of cyclooxygenase 2 (COX-2) mRNA expression and increased s

34 factor (erythroid derived-2) like2 (Nrf-2), cyclooxygenase 2 (COX-2) products, or lipoxin action.

35 flammatory agonists induce the expression of cyclooxygenase 2 (COX-2), an enzyme that catalyzes rate-

36 quires cytosolic phospholipase A2 (cPLA(2)), cyclooxygenase 2 (COX-2), and microsomal prostaglandin E

37 ound that beta-adrenergic activation induced cyclooxygenase 2 (COX-2), not COX-1, expression in a man

38 flammatory process: phospholipase A2 (PLA2), cyclooxygenase 2 (COX-2), thrombin, and transglutaminase

39 , N-acylethanolamine acid amidase (NAAA), or cyclooxygenase 2 (COX-2).

40 cytokines, which activate fibroblast via the cyclooxygenase 2 (COX-2)/prostaglandin E2 (PGE2) pathway

41 Cyclooxygenase 2 (Cox2) and mammalian target of rapamyci

42 ses and anti-oxidative enzymes by decreasing cyclooxygenase 2 (COX2) expression and restoring the act

43 n of eicosanoid (12-lipoxygenase (12-LO) and cyclooxygenase 2 (COX2))- and reactive oxygen species (N

44 protection was associated with induction of cyclooxygenase 2 and increases of its product 15-deoxy D

45 ter and expression of NF-kB-dependent genes, cyclooxygenase 2 and inducible endothelial nitric oxide

46 TRAF-6, as well as the inflammatory factors cyclooxygenase 2 and interleukin 1beta.

47 confirmed using pharmacologic inhibitors of cyclooxygenase 2 and peroxisome proliferator-activated r

48 nsaturated fatty acid oxidation by wild-type cyclooxygenase 2 and the Y334F variant, lacking a conser

49 s on prostaglandin E2 that is synthesized by cyclooxygenase 2 in neural cells.

50 level of PGE2 This was confirmed by in vivo cyclooxygenase 2 inhibition, which attenuated fungal-ind

51 e antidepressant properties of the selective cyclooxygenase 2 inhibitor celecoxib (SMD, -0.29; 95% CI

52 Treatment with a cyclooxygenase 2 inhibitor celecoxib significantly impro

53 ular risks associated with anti-inflammatory cyclooxygenase 2 inhibitors (coxibs) by targeting the pr

54 onstatin cholesterol-lowering medications or cyclooxygenase 2 inhibitors and the development of TAO.

55 -year nonvertebral fracture risk, a study of cyclooxygenase 2 inhibitors versus nonselective nonstero

56 The expression of cyclooxygenase 2 was significantly higher in kidneys fro

57 ha (tumor necrosis factor-alpha), and COX-2 (cyclooxygenase 2) are upregulated in non-occluded wounds

58 protection and determined the involvement of cyclooxygenase 2, 15-deoxy Delta-prostaglandin J2, and p

59 onal gene targets, the inflammatory mediator cyclooxygenase 2, and the matricellular protein cysteine

60 bitor or small interfering RNA or inhibiting cyclooxygenase 2, resulting in inhibition of endogenous

61 3, or enzymes like inducible NO synthase and cyclooxygenase 2, was reduced.

62 endocannabinoid, 2-arachidonoylglycerol, by cyclooxygenase 2.

63 t 15-deoxy Delta-prostaglandin J2 as well as cyclooxygenase 2/15-deoxy Delta-prostaglandin J2-depende

64 inst ventilator-induced lung injury involves cyclooxygenase 2/15-deoxy Delta-prostaglandin J2-depende

65 demonstrated that KSHV utilizes inflammatory cyclooxygenase 2/prostaglandin E2 to establish and maint

66 concomitant use of nonselective (ns)NSAIDs, cyclooxygenase -2 selective inhibitors (COX-2 inhibitors

67 ponses evoked by whisker stimulation involve cyclooxygenase-2 (COX-2) activity and activation of the

68 ther nonselective or selective inhibitors of cyclooxygenase-2 (COX-2) activity can induce or exacerba

69 However, cyclooxygenase-2 (COX-2) and angiopoietin-2 (Ang-2) were

70 l as the production of inflammatory proteins cyclooxygenase-2 (COX-2) and inducible nitric oxide synt

71 We have shown that the enzyme cyclooxygenase-2 (COX-2) and its prostanoid products, pr

72 in E2 (PGE2) synthesis pathway consisting of cyclooxygenase-2 (COX-2) and microsomal prostaglandin E

73 ediated by induced expression of the enzymes cyclooxygenase-2 (COX-2) and microsomal prostaglandin E

74 gration through increasing the expression of cyclooxygenase-2 (COX-2) and production of prostaglandin

75 , inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) and reduced cisplatin-mediated

76 Elevated cyclooxygenase-2 (COX-2) and the associated inflammation

77 as PGD2-active could serve as ligands of the cyclooxygenase-2 (COX-2) binding pocket.

78 Cyclooxygenase-2 (COX-2) catalyzes the oxygenation of ar

79 ed levels of inflammation, including greater cyclooxygenase-2 (COX-2) expression and activity in adip

80 fect, as indicated by honokiol inhibition of cyclooxygenase-2 (COX-2) expression and PGE2 production

81 This study investigated the role of cyclooxygenase-2 (COX-2) expression by donor and host ce

82 E2 (PGE2) due to their thousands-fold higher cyclooxygenase-2 (COX-2) expression than immune cells.

83 Selective silencing of the cyclooxygenase-2 (COX-2) gene with the loss of the antif

84 Purpose Tumor overexpression of cyclooxygenase-2 (COX-2) has been associated with worse

85 Cyclooxygenase-2 (COX-2) has been implicated in cell inv

86 of a high-sodium diet induces expression of cyclooxygenase-2 (COX-2) in macrophages, resulting in en

87 -regulation of heparin-binding (HB-) EGF and cyclooxygenase-2 (COX-2) in the uterine epithelium contr

88 Recent studies have suggested cyclooxygenase-2 (COX-2) inhibition could represent a no

89 In mouse models, cyclooxygenase-2 (COX-2) inhibition during involution re

90 n rodent models of postpartum breast cancer, cyclooxygenase-2 (COX-2) inhibition during the involutio

91 Cyclooxygenase-2 (COX-2) is a key enzyme in gastrointest

92 Cyclooxygenase-2 (COX-2) is activated in response to isc

93 Cyclooxygenase-2 (Cox-2) is an inducible enzyme involved

94 Cyclooxygenase-2 (COX-2) is an inducible enzyme that dri

95 rmined that oral cancer cells overexpressing cyclooxygenase-2 (COX-2) limited the cleavage of caspase

96 -1beta mRNA; BLP was more potent in inducing cyclooxygenase-2 (COX-2) mRNA and protein expression.

97 Enhanced and immediate expression of cyclooxygenase-2 (COX-2) mRNA is observed in IL-1beta-st

98 Mice were engineered to express either cyclooxygenase-2 (COX-2) or IkappaB kinase-2 (IKK2), and

99 Cyclooxygenase-2 (COX-2) overexpression is implicated in

100 Cyclooxygenase-2 (COX-2) oxygenates arachidonic acid (AA

101 Cyclooxygenase-2 (COX-2) oxygenates arachidonic acid (AA

102 cer aggressiveness through activation of the cyclooxygenase-2 (COX-2) pathway and the concomitant inc

103 crossover of the 5-lipoxygenase (5-LOX) and cyclooxygenase-2 (COX-2) pathways.

104 both enhance 15-PGDH expression and suppress cyclooxygenase-2 (COX-2) production may more effectively

105 is by directly upregulating the synthesis of cyclooxygenase-2 (COX-2) protein and activates the beta-

106 flammatory drugs selective for inhibition of cyclooxygenase-2 (COX-2) reveal an emergent cardiovascul

107 Cyclooxygenase-2 (COX-2) triggers pro-inflammatory proce

108 f inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) was decreased and the nuclear t

109 Estradiol increased the expression of cyclooxygenase-2 (COX-2), a rate-limiting enzyme in pros

110 There is accumulating evidence that cyclooxygenase-2 (COX-2), an enzyme involved in prostagl

111 nti-inflammatory drugs which directly target cyclooxygenase-2 (COX-2), an enzyme mainly responsible f

112 ar reactive oxygen species (ROS) and inhibit cyclooxygenase-2 (COX-2), an enzyme that is overexpresse

113 nverted to the unstable intermediate PGH2 by cyclooxygenase-2 (COX-2), and PGH2 undergoes an isomeriz

114 operoxide H synthase-2 (PGHS-2), also called cyclooxygenase-2 (COX-2), converts arachidonic acid to P

115 ll interactions was initiated by endothelial cyclooxygenase-2 (COX-2), increased by atorvastatin via

116 human chondrocytes induced the synthesis of cyclooxygenase-2 (COX-2), interleukin-1beta (IL-1beta) a

117 We previously reported that cyclooxygenase-2 (Cox-2)-dependent PGE2 synthesis regula

118 ammatory signals and activate, via Tpl2, the cyclooxygenase-2 (Cox-2)-prostaglandin E2 (PGE2) pathway

119 se Czeta (PKCzeta) via the infection-induced cyclooxygenase-2 (COX-2)/PGE2 axis and inducing its nucl

120 ition of the key signaling components in the cyclooxygenase-2 (COX-2)/prostaglandin E2 signaling casc

121 Cyclooxygenase-2 (COX-2, PTGS2) is an enzyme involved in

122 on, this study showed that hypoxia activated cyclooxygenase-2 (COX2) expression along with TNF-alpha.

123 r (TNBC), nitric oxide synthase-2 (NOS2) and cyclooxygenase-2 (COX2) have been described as independe

124 In addition, we simulated the effects of cyclooxygenase-2 (COX2) inhibition and C3 knockout on th

125 In vivo administration of the cyclooxygenase-2 (COX2) inhibitor celecoxib effectively

126 enhancer of activated B cells (NFkappaB) and cyclooxygenase-2 (COX2) pathways without cell death.

127 36 and endothelial nitric oxide synthase and cyclooxygenase-2 activity.

128 Inhibitors of cyclooxygenase-2 alleviate pain and reduce fever and inf

129 otes arthritis via differentially regulating cyclooxygenase-2 and arginase-1 levels.

130 s to induce NFATC2-mediated transcription of cyclooxygenase-2 and GAL.

131 ect activation of the proinflammatory factor cyclooxygenase-2 and indirect inhibition of the anti-inf

132 Betalains dampened cyclooxygenase-2 and interleukin-8 mRNA expression after

133 at cigarette smoke induces the expression of cyclooxygenase-2 and microsomal prostaglandin E synthase

134 ticancer effects may be due to inhibition of cyclooxygenase-2 and other pathways.

135 rs, OT led to increases in the expression of cyclooxygenase-2 and phosphorylated cytosolic phospholip

136 n of p38 MAPK and NF-kappaB and induction of cyclooxygenase-2 by TLR ligands, but not by IL-1beta or

137 Cyclooxygenase-2 catalyses the biosynthesis of prostagla

138 mice (P < 0.001), which exhibited decreased cyclooxygenase-2 expression and apoptosis, decreased int

139 Increased cyclooxygenase-2 expression and prostaglandin E2 release

140 KC at 6 h and decreased IL-6, TNF-alpha, and cyclooxygenase-2 expression at 24 h post infection.

141 Oxidative stress resulted in cyclooxygenase-2 expression in aortic lesions.

142 ted LPS-induced prostaglandin E2 production, cyclooxygenase-2 expression, and nuclear factor kappaB t

143 logical analysis showed that the deletion of cyclooxygenase-2 in brain endothelial cells occurred pre

144 G9a and EZH2 in the epigenetic silencing of cyclooxygenase-2 in idiopathic pulmonary fibrosis.

145 versus 2/10, P < 0.06), and upregulation of cyclooxygenase-2 in ipsilateral cortex remote from clots

146 Roles of 5-lipoxygenase and cyclooxygenase-2 in the biosynthesis of hemiketals E2 an

147 ion of the prostaglandin synthesizing enzyme cyclooxygenase-2 in the brain endothelium, generated wit

148 -1 beta, inducible nitric oxide synthase and cyclooxygenase-2 in the cortex after spreading depolariz

149 f AMP-activated protein kinase signaling and cyclooxygenase-2 increased in the ischemic myocardium of

150 ins also was decreased, whereas the level of cyclooxygenase-2 increased.

151 However, the mechanisms linking cyclooxygenase-2 inhibition and cardiovascular events ar

152 omarker and mechanistic bridge between renal cyclooxygenase-2 inhibition and systemic vascular dysfun

153 omarker and mechanistic bridge between renal cyclooxygenase-2 inhibition and systemic vascular dysfun

154 tor 2 activity, anti-oxidative activity, and cyclooxygenase-2 inhibition compared with the other samp

155 these prostaglandins, particularly PGI2, by cyclooxygenase-2 inhibition or deletion of its I prostan

156 e recurrent UTI, which could be prevented by cyclooxygenase-2 inhibition or vaccination.

157 Cardiovascular side effects associated with cyclooxygenase-2 inhibitor drugs dominate clinical conce

158 us to demonstrate that pain was blocked by a cyclooxygenase-2 inhibitor, suggesting an indirect effec

159 Cyclooxygenase-2 inhibitors (coxibs) are characterized b

160 Wild-type mice or human volunteers taking cyclooxygenase-2 inhibitors also showed increased plasma

161 same cardiovascular risk as NSAIDs with less cyclooxygenase-2 inhibitory activity, but at the cost of

162 -arachidonoyl-glycerol can be metabolized by cyclooxygenase-2 into PG-ethanolamide (PG-EA) and PG-gly

163 The cyclooxygenase-2 is a pro-inflammatory and cancer marker

164 Cyclooxygenase-2 is expressed in the renal medulla where

165 hypothalamus, as reflected in the levels of cyclooxygenase-2 mRNA, showed strong correlation with th

166 th epilepsy, and is attenuated by inhibiting cyclooxygenase-2 or L-type calcium channels.

167 ed cells was induced by CSF2 rather than the cyclooxygenase-2 pathway, and treatment of monocyte-deri

168 fined daily dose >/=0.3) of agents with high cyclooxygenase-2 selectivity (OR, 0.57 [CI, 0.44 to 0.74

169 denosine receptor antagonism and blockade of cyclooxygenase-2 signaling, and partially reproduced by

170 ith expression of IL-6, TNF-alpha, IL-8, and cyclooxygenase-2 was also investigated.

171 Transcriptome analysis of wild-type and cyclooxygenase-2(-/-) mouse tissues revealed 1 gene alte

172 endoperoxide synthase 2 expression (PTGS2 or cyclooxygenase-2), measured in 245 tumor samples by immu

173 se EZH2 (enhancer of zeste homolog 2), COX2 (cyclooxygenase-2), POMP (proteasome maturation protein),

174 udies support a carcinogenic role for PTGS2 (cyclooxygenase-2), which is an important enzymatic media

175 pression of early growth response protein 1, cyclooxygenase-2, and brain-derived neurotrophic factor

176 reduced nuclear factor-kappaB translocation, cyclooxygenase-2, and phosphoextracellular signal-regula

177 Nuclear factor-kappaB translocation, cyclooxygenase-2, and phosphoextracellular signal-regula

178 r desmin were lost, along with expression of cyclooxygenase-2, and the number of vimentin-positive ce

179 downstream prolabor gene expression, such as cyclooxygenase-2, C-C motif chemokine ligand 2, interleu

180 Microglial cyclooxygenase-2, microsomal PGE synthase, and PGE2 expr

181 row transplant (BMT) neutrophils overexpress cyclooxygenase-2, overproduce prostaglandin E2 (PGE2), a

182 ss (P <0.05), as well as increased levels of cyclooxygenase-2, serum C-terminal telopeptide (CTX), p3

183 n vascular cells that also express inducible cyclooxygenase-2, suggesting that such cells are the sou

184 , the proangiogenic and antiapoptotic enzyme cyclooxygenase-2, the IL-8 receptor C-X-C chemokine rece

185 Administration of an inhibitor to cyclooxygenase-2, the initiating enzyme in the RvT pathw

186 mPGES-1-positive cells, was coexpressed with cyclooxygenase-2, whereas there was no coexpression betw

187 more, in mice with a history of chronic UTI, cyclooxygenase-2-dependent inflammation allowed a variet

188 r bacterial colonization, and (3) changes to cyclooxygenase-2-dependent inflammation.

189 Further, we show that the cyclooxygenase-2-dependent lipid inflammatory pathway is

190 ation of TLR4 results in accumulation of the cyclooxygenase-2-derived lipoxin precursor 15-hydroxyeic

191 nflammatory drugs specific for inhibition of cyclooxygenase-2.

192 hway that induced the proinflammatory enzyme cyclooxygenase-2.

193 as previously under-appreciated products of cyclooxygenase-2.

194 rdiovascular disease, highlights the role of cyclooxygenase-2/microsomal PGE synthase 1/PGE2 signalin

195 ng and with Tyr-385 and Ser-530 close to the cyclooxygenase active site, interfering in enzyme cataly

196 CD4(+) T cells was reduced by inhibitors of cyclooxygenase and 12-lipoxygenase, which metabolize ara

197 ed by iPLA2beta and subsequently oxidized by cyclooxygenase and 12-LO favor macrophage inflammatory M

198 variants further influence pro-inflammatory, cyclooxygenase and lipoxygenase eicosanoid products.

199 Cyclooxygenase and lipoxygenase metabolites prostaglandi

200 which may be mediated through the impact on cyclooxygenase and lipoxygenase pathways.

201 contains the signature catalytic sequence of cyclooxygenases and fungal linoleate dioxygenases (YRWH)

202 C-PUFA metabolites from 2 groups of enzymes, cyclooxygenases and lipoxygenases, inhibit [and the omeg

203 o ischemia-reperfusion injury is mediated by cyclooxygenases and that their inhibition may be associa

204 t selectivity over related lipoxygenases and cyclooxygenases, and possess favorable ADME properties.

205 alkynyl arachidonic acid in the tracking of cyclooxygenase-based lipid oxidation.

206 revealed that the inhibitor binds within the cyclooxygenase channel in an inverted orientation, with

207 -stabilizing agents and/or inhibitors of the cyclooxygenase (COX) and 5-lipoxygenase (5-LOX) pathways

208 Arachidonic acid (ARA) is metabolized by cyclooxygenase (COX) and cytochrome P450 to produce proa

209 of AA and LA by mammalian enzymes including cyclooxygenase (COX) and lipoxygenase (LOX) has revealed

210 Kinetic models were developed for the cyclooxygenase (COX) and lipoxygenase branches of arachi

211 te that PSaV induced the vitalization of the cyclooxygenase (COX) and prostaglandin E2 (PGE2) pathway

212 Cyclooxygenase (COX) catalyzes the first step in prostan

213 In young adults, cyclooxygenase (COX) contributes to the heat loss respon

214 Cyclooxygenase (COX) contributes to the regulation of cu

215 (PGs)--lipid signals produced downstream of cyclooxygenase (COX) enzymes--regulate actin dynamics in

216 We have previously reported that cyclooxygenase (COX) inhibition by indomethacin augmente

217 The aim of this study was to analyze if cyclooxygenase (COX) inhibitors could improve the early

218 Culture of T. suis with several cyclooxygenase (COX) inhibitors that inhibit mammalian p

219 release from human macrophages compared with cyclooxygenase (COX) inhibitors.

220 Prostaglandins derived from the cyclooxygenase (COX) pathway and epoxyeicosatrienoic aci

221 lthough NF-kappaB and AP-1 are involved, the cyclooxygenase (COX) pathway is the dominant regulator o

222 atory lipid mediators synthesized across the cyclooxygenase (COX), lipoxygenase (LOX), and cytochrome

223 Cyclooxygenase (COX)-1 and -2 catalyze the first step in

224 anti-inflammatory drugs (NSAIDs) to inhibit cyclooxygenase (Cox)-1 and Cox-2 underlies the therapeut

225 oduction of prostaglandins I2 and E2 through cyclooxygenase (COX)-1 and regulates gene expression by

226 Inactivation of platelet cyclooxygenase (COX)-1 by low-dose aspirin leads to long

227 ic deletion or pharmacological inhibition of cyclooxygenase (COX)-2 abrogates intestinal adenoma deve

228 ced induction of the proinflammatory protein cyclooxygenase (COX)-2 and the proinflammatory cytokines

229 Cyclooxygenase (COX)-2 has been shown to be involved in

230 e role of transcription factor NF-kappaB and cyclooxygenase (COX)-2 in ketamine-induced cystitis.

231 matrix metalloproteinase (MMP)-8, IL-6, and cyclooxygenase (COX)-2 messenger RNAs (mRNAs) were evalu

232 We analyzed whether cyclooxygenase (COX)-2 signaling regulates this vasculog

233 at this association is stronger with greater cyclooxygenase (cox)-2 when compared with cox-1 inhibiti

234 induce NOD2-dependent immunomodulators like cyclooxygenase (COX)-2, suppressor of cytokine signaling

235 , including inducible NO synthase (iNOS) and cyclooxygenase (COX)-2.

236 e their antiinflammatory effects by blocking cyclooxygenase (COX)-2.

237 (anti-inflammatory; M2/AAM) phenotype, where cyclooxygenase (COX)-dependent cyclopentenone prostaglan

238 We present evidence that the cyclooxygenase (COX)-derived eicosanoid prostaglandin E2

239 Cyclooxygenase (COX)-derived oxylipins are important med

240 Cyclooxygenase (COX)-inhibiting drugs augmented allergic

241 mulates prostaglandin-endoperoxide synthase [cyclooxygenase (Cox)]-independent prostaglandin synthesi

242 , inducible nitric oxide synthase (iNOS) and cyclooxygenase (COX-2) inhibitory activity than an equiv

243 anti-inflammatory drug (NSAID) that inhibits cyclooxygenases (COX) -1 and -2.

244 rachidonic acid by the sequential actions of cyclooxygenases (COX) and PGE synthases (PTGES).

245 Genetic ablation of cyclooxygenases (COX) or prostaglandin E synthases in Br

246 Eicosanoids, including PGs, produced by cyclooxygenases (COX), and leukotrienes, produced by 5-l

247 e interaction with their target enzymes, the cyclooxygenases (COX).

248 in synthesis through the activation of PLA2, cyclooxygenases (COX-1 and -2) and prostaglandins and at

249 staglandin-endoperoxide synthase 1 (PTGS1 or cyclooxygenase [COX] 1) and PTGS1 (COX2), other factors

250 Two cyclooxygenases, COX-1 and COX-2, catalyze the initial s

251 Cyclooxygenases (COXs) and their final product, prostagl

252 Cyclooxygenases (COXs) catalyze the committed step in pr

253 ndoperoxide H synthases (PGHSs), also called cyclooxygenases (COXs), convert arachidonic acid (AA) to

254 essor of neutrophil functions, the impact of cyclooxygenase-derived endocannabinoids such as PGE2-EA

255 relied upon the endogenous production of the cyclooxygenase-derived prostaglandins Delta(12)-PGJ2 and

256 his present study, we determined the role of cyclooxygenase-derived prostanoids in this contractile r

257 The cyclooxygenase enzyme inhibitory activity of extract and

258 Cyclooxygenase enzymes (COX-1 and COX-2) catalyze the co

259 l anti-inflammatory drugs, which inhibit the cyclooxygenase enzymes COX-1 and COX-2, reduce the risk

260 flammatory activity as confirmed by in vitro cyclooxygenase enzymes inhibitory assays.

261 he oldest and most widely used drugs such as cyclooxygenase inhibiting NSAIDs, whereas others remain

262 Also, cyclooxygenase inhibition by anthocyanins was stimulated

263 her, these data demonstrate broad effects of cyclooxygenase inhibition on multiple neuronal pathways

264 the effects of achieving faster and stronger cyclooxygenase inhibition with intravenous lysine acetyl

265 ated with combined nitric oxide synthase and cyclooxygenase inhibition.

266 a signaling as a novel therapeutic target of cyclooxygenase inhibition.

267 e prevented by peripheral treatment with the cyclooxygenase inhibitor nimesulide or the aromatase inh

268 nflammatory compound indomethacin, a general cyclooxygenase inhibitor, affected obesity development a

269 Indomethacin, a cyclooxygenase inhibitor, countered the ICC-SC-mediated

270 bitor, (R)-bromoenol lactone, but not by the cyclooxygenase inhibitor, indomethacin.

271 spore germination and mycelial growth by two cyclooxygenase inhibitors (aspirin and indomethacin) als

272 a difference in pain reduction compared with cyclooxygenase inhibitors and glucocorticoids for treati

273 Suppression of PGE(2) synthesis by the cyclooxygenase inhibitors aspirin and celecoxib suppress

274 pound 1 also showed clear superiority to the cyclooxygenase inhibitors diclofenac and rofecoxib.

275 w potential applications of these identified cyclooxygenase inhibitors in preventing inflammatory dis

276 action, which was partially inhibited by the cyclooxygenase inhibitors indomethacin and flurbiprofen.

277 nchoconstriction in response to nonselective cyclooxygenase inhibitors that deplete homeostatic PGE2.

278 fen, ibuprofen, diclofenac, ketorolac, etc., cyclooxygenase inhibitors) as agents for the management

279 NSAIDs) associated with better outcomes than cyclooxygenase inhibitors, glucocorticoids, IL-1 inhibit

280 T was rescued both in vitro and in vivo with cyclooxygenase inhibitors.

281 thdrawal due to adverse events compared with cyclooxygenase inhibitors.

282 ifty lipid species, including metabolites of cyclooxygenases, lipoxygenases, epoxygenases, and other

283 Burgeoning evidence supports a role for cyclooxygenase metabolites in regulating membrane excita

284 mphoma (cHL), a process that is regulated by cyclooxygenase/nuclear factor-kappaB/activator protein 1

285 nists of nuclear factor kappa B (NF-kappaB), cyclooxygenase pathway and melanocortin receptors 3/4 re

286 transcripts involving both lipoxygenase and cyclooxygenase pathways are increased in smokers with as

287 Possibly targeting specific lipoxygenase and cyclooxygenase pathways that are activated by asthma and

288 dent inhibition of production of vasodilator cyclooxygenase products or O2 -dependent destruction of

289 This study has identified that the cyclooxygenase products thromboxane and PGF2alpha are re

290 ne B4, and 5-HETE but no effect on levels of cyclooxygenase products.

291 Cyclooxygenase-prostaglandin (PG) E2 signaling within th

292 The inflammatory cyclooxygenase/prostaglandin E2 (COX/PGE2) pathway has b

293 vel interactions between three drugs and the cyclooxygenase proteins predicted by DTINet, and demonst

294 tenone metabolite, 15d-PGJ2, produced by the cyclooxygenase (Ptgs; Cox) pathway.

295 The S-enantiomer inhibits cyclooxygenases; R-ketorolac is a selective inhibitor of

296 scriptional regulation of the enzymes of the cyclooxygenase routes, where PGE2 is the most relevant p

297 e to inhibit phospholipase, lipoxygenase and cyclooxygenase, three pro-inflammatory enzymes.

298 Dutasteride also induces cyclooxygenase type 2 (COX-2), which functions in a nega

299 tion, whereas the irreversible inhibition of cyclooxygenase with aspirin increased the parasite burde

300 n was the most potent in the inactivation of cyclooxygenase, with a reduction of 32% of the control a