ライフサイエンスコーパス: cyclooxygenase

1 ed activation of endothelial NO synthase and cyclooxygenase.

2 The highest inhibition of activities of cyclooxygenase 1 and -2, as well as amylase and glucosid

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

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

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

6 ioactive lipids derived from the activity of cyclooxygenase-1 (COX-1) and COX-2.

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

8 neration may reduce the duration of platelet cyclooxygenase-1 (COX-1) inhibition.

9 ibed a new bioactive eicosanoid generated by cyclooxygenase-1 (COX-1) turnover during platelet activa

10 Cyclooxygenase-1 (COX-1), a biomarker for neuroinflammat

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

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

13 141.6 and 138.8 muM, respectively) inhibited cyclooxygenase-1 and -2 enzymes by 50%.

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

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

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

17 rsor RNA, H19, correlated with expression of cyclooxygenase-1 and cyclooxygenase-2 and shorter surviv

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

21 que ability to irreversibly inhibit platelet cyclooxygenase-1 is a key mechanism by which aspirin exe

22 imulus, this reaction is catalyzed by either cyclooxygenase-1 or cyclooxygenase-2 (COX-1 or COX-2).

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

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

25 d an intolerance of medications that inhibit cyclooxygenase-1.

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

27 roxide H synthases-1 and -2, commonly called cyclooxygenases-1 and -2 (COX-1 and -2), catalyze the co

28 of alpha-glucosidase, alpha-amylase, lipase, cyclooxygenases-1 and -2 (COX-1/COX-2), and lipoxygenase

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

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

31 The overexpression of cyclooxygenase 2 (COX-2) gene, also known as prostagland

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

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

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

35 exhibit more wound myofibroblasts and fewer cyclooxygenase 2 (Cox-2)-positive dermal cells than cont

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

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

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

39 nking oxidative stress with the induction of cyclooxygenase 2 (COX2) in an ATF4-dependent manner.

40 Interestingly, a 10-day treatment with the cyclooxygenase 2 (COX2) inhibitor ibuprofen (30 mg/kg bo

41 Selective cyclooxygenase 2 (COX2) inhibitors (also known as coxibs

42 Cyclooxygenase 2 (Cox2) total knockout and myeloid knock

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 Treatment with a cyclooxygenase 2 inhibitor celecoxib significantly impro

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

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

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

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

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

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

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

59 The pathways then diverge into a cyclooxygenase 2-mediated and a lipoxygenase-mediated ro

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

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

62 type ECs, FSS elicited a marked rise in COX (cyclooxygenase)-2 and L-PGDS (lipocalin-type prostagland

63 n is catalyzed by either cyclooxygenase-1 or cyclooxygenase-2 (COX-1 or COX-2).

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

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

66 t KSHV infection hijacks the proinflammatory cyclooxygenase-2 (COX-2) and 5-lipoxygenase (5-LO) pathw

67 c acid metabolism pathways, specifically the cyclooxygenase-2 (COX-2) and 5-lipoxygenase (5-LOX) path

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

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

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

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

72 t combined pharmacological abrogation of the cyclooxygenase-2 (COX-2) and soluble epoxide hydrolase (

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

74 We previously demonstrated that cyclooxygenase-2 (COX-2) and the prostaglandin E recepto

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

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

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

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

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

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

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

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

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

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

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

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

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

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

89 Cyclooxygenase-2 (COX-2) is elevated in skin, dorsal roo

90 Cyclooxygenase-2 (COX-2) is involved in different liver

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

92 -1beta mRNA; BLP was more potent in inducing cyclooxygenase-2 (COX-2) mRNA and protein expression.

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

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

95 Cyclooxygenase-2 (COX-2) overexpression is prominent in

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

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

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

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

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

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

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

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

104 ases expression of the protumorigenic factor cyclooxygenase-2 (COX-2), and that COX-2 inhibition enha

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

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

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

108 ) and glutelin (n = 17) had interaction with cyclooxygenase-2 (COX-2), p65- nuclear factor kappa B, l

109 storm." AFB(1)-generated debris up-regulates cyclooxygenase-2 (COX-2), soluble epoxide hydrolase (sEH

110 Many indomethacin amides and esters are cyclooxygenase-2 (COX-2)-selective inhibitors, providing

111 te-limiting enzyme in PGE2 synthesis-namely, cyclooxygenase-2 (COX-2).

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

113 dulla, including Wnt/beta-catenin signaling, cyclooxygenase-2 (COX-2)/prostaglandin E(2) (PGE(2) ) si

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

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

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

117 out of the EP4 gene in the sensory nerves or cyclooxygenase-2 (COX2) in the osteoblastic cells signif

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

119 36 and endothelial nitric oxide synthase and cyclooxygenase-2 activity.

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

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

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

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

124 ted the expression of inducible NO synthase, cyclooxygenase-2 and interleukin-1beta.

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

126 i-inflammatory activities through inhibiting cyclooxygenase-2 and lipoxygenase activities, particular

127 i-inflammatory activities through inhibiting cyclooxygenase-2 and lipoxygenase activity.

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

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

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

131 ated with expression of cyclooxygenase-1 and cyclooxygenase-2 and shorter survival times of patients

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

133 Cyclooxygenase-2 catalyses the biosynthesis of prostagla

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

135 In addition, Sch A decreased the DON-induced cyclooxygenase-2 expression and prostaglandin E2 product

136 Increased cyclooxygenase-2 expression and prostaglandin E2 release

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

138 din EP4 receptor attenuates the induction of cyclooxygenase-2 expression by EP2 receptor activation i

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

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

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

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

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

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

145 -1 beta, inducible nitric oxide synthase and cyclooxygenase-2 in the cortex after spreading depolariz

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

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

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

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

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

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

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

153 ntake; administration of NS-398, a selective cyclooxygenase-2 inhibitor, abolished the arterial press

154 y simultaneous adolescent treatment with the cyclooxygenase-2 inhibitor, NS398.

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

156 Cyclooxygenase-2 inhibitors (coxibs) are characterized b

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

158 ophen, nonsteroidal anti-inflammatory drugs, cyclooxygenase-2 inhibitors, gabapentinoids, and ketamin

159 ophen, nonsteroidal anti-inflammatory drugs, cyclooxygenase-2 inhibitors, gabapentinoids, ketamine, p

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

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

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

163 Cyclooxygenase-2 is expressed in the renal medulla where

164 Differential and exacerbated expressions of cyclooxygenase-2 might be the cause of excessive neurona

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 stically activated the nuclear factor-kappaB-cyclooxygenase-2 pathway in astrocytes and decreased imm

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

169 Kidney cyclooxygenase-2 protein levels were increased in Pkd1 k

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

171 to suppression of the Akt/NF-kappaB-mediated cyclooxygenase-2 signaling pathway.

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

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

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

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

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

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

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

179 L)-1beta, IL-6, tumor necrosis factor-alpha, cyclooxygenase-2, and phosphorylated NF-kappaB, as well

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

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

182 We found that PTGS2, the gene encoding cyclooxygenase-2, lies downstream of EPHA2 signaling thr

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

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

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

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

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 the association of gastric acid stress with Cyclooxygenase-2-dependent tumor formation originating f

191 er status epilepticus (SE), driven partly by cyclooxygenase-2-mediated activation of prostaglandin EP

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

193 nflammatory drugs specific for inhibition of cyclooxygenase-2.

194 hway that induced the proinflammatory enzyme cyclooxygenase-2.

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

196 ory mediators of Infgamma, Litaf, and Ptgs2 (Cyclooxygenases-2 (COX-2) gene) in chicken splenocytes.

197 Residual cyclooxygenase activity of aspirin-acetylated COX-2 form

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

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

200 Cyclooxygenase and lipoxygenase metabolites prostaglandi

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

202 rate with a dye precursor to engage both the cyclooxygenase and peroxidase activities of COX-2.

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

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

205 ith known inhibitors of histone deacetylase, cyclooxygenase, and pyruvate dehydrogenase kinase.

206 We identify key structural features of the cyclooxygenases, break down their active site into regio

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

208 its acetyl group to a serine residue in the cyclooxygenase (COX) active site.

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

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

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

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

213 Cyclooxygenase (COX) catalyzes the first step in prostan

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

215 Cyclooxygenase (COX) contributes to the regulation of cu

216 The effects of cyclooxygenase (COX) inhibition and PG assays indicate t

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

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

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

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

221 The cyclooxygenase (COX) metabolic pathway regulates immune

222 rily target the 5-lipoxygenase (5-LO) or the cyclooxygenase (COX) pathways, very few compounds select

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

224 d (EPA), and (2) the enzyme group, including cyclooxygenase (COX), lipoxygenase (LOX), or cytochrome

225 n prevents thrombosis by inhibiting platelet cyclooxygenase (COX)-1 activity and the production of th

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

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

228 eroidal anti-inflammatory drugs that inhibit cyclooxygenase (COX)-1 and COX-2, increases heart failur

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

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

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

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

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

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

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

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

237 eta, inducible nitric oxide synthase (iNOS), cyclooxygenase (COX)-2, matrix metalloproteinase (MMP)-9

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

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

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

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

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

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

249 Cyclooxygenases (COXs) and their final product, prostagl

250 Cyclooxygenases (COXs) catalyze the committed step in pr

251 prostaglandins and leukotrienes by targeting cyclooxygenases (COXs), 5-lipoxygenase (LOX), or the 5-L

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

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

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

255 The cyclooxygenase enzyme inhibitory activity of extract and

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

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

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

259 inflammatory drugs (NSAIDs) target primarily cyclooxygenase enzymes, a subset of NSAIDs containing ca

260 ally modulated, functional heterodimers, the cyclooxygenases exhibit complex kinetic behavior, requir

261 is mediated by the discordant expression of cyclooxygenase genes in epithelial cells and regulated b

262 the part of the pharmaceutical industry, the cyclooxygenases have been the focus of a vast array of s

263 osal cells is elusive because of the diverse cyclooxygenase-independent effects of these drugs.

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

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

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

267 ated with combined nitric oxide synthase and cyclooxygenase inhibition.

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

269 The cyclooxygenase inhibitor indomethacin completely abolish

270 is reduced by gabapentin but not the potent cyclooxygenase inhibitor ketorolac.

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

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

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

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

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

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

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

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

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

280 different nonopioid analgesic drug classes (cyclooxygenase inhibitors, acetaminophen, nefopam, or me

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

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

283 thdrawal due to adverse events compared with cyclooxygenase inhibitors.

284 Pxt is the Drosophila cyclooxygenase-like enzyme responsible for PG synthesis.

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

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

287 Gs with indomethacin or HQL79, which inhibit cyclooxygenases or hematopoietic prostaglandin D synthas

288 novel metabolites generated from the direct cyclooxygenase- or lipoxygenase-catalyzed oxidation of 2

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

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

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

292 Cyclooxygenase-prostaglandin (PG) E2 signaling within th

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

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

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

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

297 ugh the generation of prostaglandins via the cyclooxygenase system.

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

299 view, we explore the chemical biology of the cyclooxygenases through the lens of this wealth of struc

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