ライフサイエンスコーパス: cyclooxygenase-2

1 endocannabinoid, 2-arachidonoylglycerol, by cyclooxygenase 2.

2 two systems, benzamidine/trypsin and SC-558/cyclooxygenase 2.

3 c oxide synthase, but enhanced expression of cyclooxygenase 2.

4 nflammatory drugs specific for inhibition of cyclooxygenase-2.

5 hway that induced the proinflammatory enzyme cyclooxygenase-2.

6 enhance eCB signalling via an inhibition of cyclooxygenase-2.

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

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

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

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

11 ase compared with pyramidal cells expressing cyclooxygenase-2 (22%, p < 0.05) or vasoactive intestina

12 e (66.7%, 65.1% and 88.0%, respectively) and cyclooxygenase-2 (62.0%, 69.9% and 40.6%, respectively).

13 36 and endothelial nitric oxide synthase and cyclooxygenase-2 activity.

14 This suggests that cyclooxygenase-2 acts downstream of the PAF-R in mediati

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

16 The Gln-ind cells overexpressed cyclooxygenase-2, an indicator of tumor aggressiveness,

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

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

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

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

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

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

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

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

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

26 din motifs 5 and of the inflammatory factors cyclooxygenase-2 and inducible nitric oxide synthase.

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

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

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

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

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

32 , and matrix metalloproteinase-2 protein and cyclooxygenase-2 and mPGES-1 mRNA expression.

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

34 ase of TNF-alpha and subsequent induction of cyclooxygenase-2 and PGE(2) engagement of EP4 receptor.

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

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

37 een characterized by increased expression of cyclooxygenase-2 and the inactivation of COX-2 prior to

38 molecule-1, inducible nitric oxide synthase, cyclooxygenase-2) and a MyD88-independent interferon reg

39 ous gene products that mediate inflammation (cyclooxygenase-2) and matrix degradation (matrix metallo

40 nitric oxide synthase), Ptgs2 (which encodes cyclooxygenase 2), and Tnf, that were primarily produced

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

42 ting cell nuclear antigen, NF-kappabeta/p50, cyclooxygenase-2, and androgen receptor was also seen.

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

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

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

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

47 n of proinflammatory molecules such as IL-6, cyclooxygenase-2, and prostacyclin, as determined by ELI

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

49 ate neighboring upstream gene, annotated as "cyclooxygenase-2," appeared to be a potential fatty acid

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

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

52 doperoxide synthase 2 (PTGS2) (also known as cyclooxygenase-2) by aspirin down-regulates phosphatidyl

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

54 Cyclooxygenase-2 catalyses the biosynthesis of prostagla

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

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

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

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

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

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

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

62 Cyclooxygenase 2 (COX-2) is an inflammatory enzyme invol

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

64 1-h treatment with thrombin or S1P increases cyclooxygenase 2 (COX-2) mRNA levels approximately 10-fo

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

66 s a key player in Derlin-1- and p97-mediated cyclooxygenase 2 (COX-2) ubiquitination and degradation.

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

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

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

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

71 Suppression of cyclooxygenase 2 (COX-2)-derived prostacyclin (PGI(2)) i

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

73 Prostaglandin production is catalyzed by cyclooxygenase 2 (cox-2).

74 f inducible nitric oxide synthase (iNOS) and cyclooxygenase 2 (COX-2).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

92 t of neurotransmitter release is mediated by cyclooxygenase-2 (COX-2) as it converts 2-AG to the glyc

93 uction is largely dependent on production of cyclooxygenase-2 (COX-2) because its inhibition in these

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

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

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

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

98 ) induces both nuclear beta-catenin-mediated cyclooxygenase-2 (COX-2) expression and prostaglandin E2

99 We evaluated cyclooxygenase-2 (COX-2) expression and the signaling pa

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

101 Cyclooxygenase-2 (COX-2) expression is induced by mitoge

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

103 Our data revealed that cyclooxygenase-2 (COX-2) expression was increased follow

104 f inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) expression, but has no effect o

105 s a key role in carcinogenesis by regulating cyclooxygenase-2 (COX-2) expression.

106 evelop topical gels that selectively inhibit cyclooxygenase-2 (COX-2) for the management of local inf

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

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

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

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

111 d mediators, mainly PGE(2) with induction of cyclooxygenase-2 (COX-2) in the lungs.

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

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

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

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

116 tudy examined the effectiveness of selective cyclooxygenase-2 (COX-2) inhibition on reducing AAA prog

117 imilar to--as well as in conjunction with--a cyclooxygenase-2 (COX-2) inhibitor, which suggests that

118 With interest waning in the use of cyclooxygenase-2 (COX-2) inhibitors for inflammatory dis

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

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

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

122 Cyclooxygenase-2 (COX-2) is an inducible enzyme that con

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

124 ted expression of the prostaglandin synthase cyclooxygenase-2 (COX-2) is commonly observed in many ch

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

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

127 The enzyme cyclooxygenase-2 (COX-2) is rapidly and transiently up-r

128 culture and increases lipid peroxidation and cyclooxygenase-2 (COX-2) levels in cultured keratinocyte

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

130 -1beta mRNA; BLP was more potent in inducing cyclooxygenase-2 (COX-2) mRNA and protein expression.

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

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

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

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

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

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

137 Cyclooxygenase-2 (COX-2) oxygenates arachidonic acid to

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

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

140 The enzyme cyclooxygenase-2 (COX-2) plays an important role in the

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

142 we identify RNA transcripts that overlap the cyclooxygenase-2 (COX-2) promoter and contain two adjace

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

144 The objective of this study is to compare cyclooxygenase-2 (COX-2) protein expression in gingival

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

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

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

148 pro-inflammatory stimuli in the brain induce cyclooxygenase-2 (COX-2), a key enzyme in arachidonic ac

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

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

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

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

153 9)-THC) are associated with the induction of cyclooxygenase-2 (COX-2), an inducible enzyme that conve

154 Expression of interleukin-8 (IL-8), cyclooxygenase-2 (COX-2), and heme oxygenase-1 (HO-1) mR

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

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

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

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

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

160 eroxide H synthase-2 (PGHS-2), also known as cyclooxygenase-2 (COX-2), is a sequence homodimer.

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

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

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

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

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

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

167 ascular endothelial growth factor (VEGF) and cyclooxygenase-2 (COX-2).

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

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

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

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

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

173 Cyclooxygenase 2 (Cox2) and mammalian target of rapamyci

174 nfected Mvarphis inhibited the expression of cyclooxygenase 2 (COX2) and microsomal prostaglandin E s

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

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

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

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

179 Cyclooxygenase 2 (Cox2) total knockout and myeloid knock

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

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

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

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

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

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

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

187 diet, and the accompanying up-regulation of cyclooxygenase-2 (COX2), increases Kras activity during

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

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

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

191 volving EP2 and EP4 prostaglandin receptors, cyclooxygenase-2-dependent reactive oxygen species produ

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

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

194 aspirin and statins) via the modification of cyclooxygenase-2 enzymatic activity.

195 acetate extracts of strawberry guavas showed cyclooxygenase-2 enzyme inhibitory activities of 18.3% a

196 ithin minutes of C. albicans addition before cyclooxygenase 2 expression.

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

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

199 Increased cyclooxygenase-2 expression and prostaglandin E2 release

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

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

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

203 per day) reduced the level of AngII-induced cyclooxygenase-2 expression in apoE(-/-)/betaarr2(+/+) m

204 ent study, we determined whether MMP-induced cyclooxygenase-2 expression was coupled to the expressio

205 effects on NF-kappaB activation and iNOS and cyclooxygenase-2 expression were not affected in LPS-sti

206 ction, increased aortic cyclooxygenase-1 and cyclooxygenase-2 expression, and increased thromboxane A

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

208 ased hyperfiltration, decreased macula densa cyclooxygenase-2 expression, decreased albuminuria, decr

209 -1) is an inducible enzyme that couples with cyclooxygenase-2 for the biosynthesis of PGE2.

210 lates the effects of conditional ablation of cyclooxygenase-2 from principal forebrain neurons, namel

211 ect on iNOS (inducible NO synthase) and COX (cyclooxygenase)-2 gene expression at transcriptional lev

212 NF-kappaB translocation and IL-6, IL-8, and cyclooxygenase-2 gene expression indicated that the prot

213 lls) activation and expression of the COX-2 (cyclooxygenase 2) gene.

214 of TNF-alpha, inducible NO synthase (iNOS), cyclooxygenase-2, IL-1beta, and IL-12.

215 one and confirmed by protein measurements of cyclooxygenase-2, IL-6, IL-10, and TNF-alpha.

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

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

218 in association with decreased expression of cyclooxygenase-2 in HIF-1alpha-deficient myeloid cells.

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

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

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

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

223 -1 beta, inducible nitric oxide synthase and cyclooxygenase-2 in the cortex after spreading depolariz

224 infiltrate and slightly higher expression of cyclooxygenase-2 in the females with these adverse pregn

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

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

227 ed the rapid up-regulation of mRNAs encoding cyclooxygenase-2, inducible NOS, IL-6, and IL-1beta but

228 ellular signal-regulated kinase 1/2-mediated cyclooxygenase-2 induction and increased inflammation.

229 olated macrophages, palmitic acid stimulated cyclooxygenase-2 induction and prostanoid production.

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

231 ity of PIK3CA mutation for benefit from both cyclooxygenase-2 inhibition and aspirin.

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

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

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

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

236 In addition, cyclooxygenase-2 inhibition did not block PAF-R agonist

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

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

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

240 Treatment with a cyclooxygenase 2 inhibitor celecoxib significantly impro

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

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

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

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

245 and this induction could be antagonized by a cyclooxygenase-2 inhibitor.

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

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

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

249 Cyclooxygenase-2 inhibitors (coxibs) are characterized b

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

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

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

253 epidermal growth factor receptor inhibitors, cyclooxygenase-2 inhibitors, green tea extract, and pero

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

255 cule-1), inducible nitric oxide synthase and cyclooxygenase-2, interferon regulatory factor-1, interf

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

257 or necrosis factor-alpha, interleukin-1beta, cyclooxygenase 2, intracellular adhesion molecule 1, and

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

259 Cyclooxygenase-2 is expressed in the renal medulla where

260 roinflammatory conditions, the expression of cyclooxygenase-2 leads to the release of large amounts o

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

262 In the presence of aspirin, acetylated cyclooxygenase-2 loses the activity required to synthesi

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

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

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

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

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

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

269 iency attenuated AngII-induced expression of cyclooxygenase-2, monocyte chemoattractant protein-1, ma

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

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

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

273 Pharmacological blockade of cyclooxygenase-2 or of prostaglandin D synthase prevente

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

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

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

277 ent macrophages revealed upregulation of the cyclooxygenase 2-peroxisome proliferator-activated-gamma

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

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

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

281 zyme, prostaglandin-endoperoxide-synthase-2/ cyclooxygenase-2 (PTGS2/COX-2), are elevated in actively

282 t of PGE(2) reflects the balance between its cyclooxygenase 2-regulated synthesis and 15-hydroxyprost

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

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

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

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

287 nhibiting nuclear factor kappa B (NF-kappaB)/cyclooxygenase 2 signaling in IR-stressed livers.

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

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

290 rostaglandin-endoperoxide synthase 2 (PTGS2, cyclooxygenase 2), suggesting that BRAF-mutant colonic c

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

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

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

294 , the nuclear factor kappaB p65 subunit, and cyclooxygenase 2; they also up-regulated expression of m

295 e effects of 2-AG through its oxygenation by cyclooxygenase-2 to give rise to the anti-inflammatory p

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

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

298 3, or enzymes like inducible NO synthase and cyclooxygenase 2, was reduced.

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

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