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 of both inducible nitric oxide synthase and cyclooxygenase 2.

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

6 n of prostacyclin proceeds in the absence of cyclooxygenase-2.

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

8 nflammatory drugs specific for inhibition of cyclooxygenase-2.

9 hway that induced the proinflammatory enzyme cyclooxygenase-2.

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

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

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

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

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

15 36 and endothelial nitric oxide synthase and cyclooxygenase-2 activity.

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

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

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

19 ing prostaglandin E2, which is downstream of cyclooxygenase 2 and a target of indomethacin.

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

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

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

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

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

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

26 d confer neuroprotection; and determined how cyclooxygenase-2 and cytokines were mechanistically-link

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

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

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

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

31 physiological cartilage aggrecanase, and of cyclooxygenase-2 and microsomal prostaglandin E synthase

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

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

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

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

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

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 e genes (oxytocin receptor, connexin 43, and cyclooxygenase-2) and prolactins are down-regulated in p

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

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

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

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

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

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

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 d to be defective in their ability to induce cyclooxygenase-2, and therefore unable to up-regulate PG

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

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

52 mmatory macrophages, expression of inducible cyclooxygenase 2, as well as proinflammatory monocyte ch

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

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

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

56 Cyclooxygenase-2 catalyses the biosynthesis of prostagla

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

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

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

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

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

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

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

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

65 1-h treatment with thrombin or S1P increases cyclooxygenase 2 (COX-2) mRNA levels approximately 10-fo

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

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

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

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

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

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

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

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

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

75 e-inducible nitric oxide synthase (iNOS) and cyclooxygenase 2 (COX-2).

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

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

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 in levels of IL-1beta, NF-kappabeta/p65, and cyclooxygenase-2 (COX-2) also were observed after treatm

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

82 ncreased expression of erythropoietin (EPO), cyclooxygenase-2 (COX-2) and angiopoietin-2 (Ang-2).

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

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

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

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

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

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

95 terized by abundant fibrillar collagen, high cyclooxygenase-2 (COX-2) expression and an invasive phen

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

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

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

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

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

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

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

103 Diabetic nephropathy (DN) increases podocyte cyclooxygenase-2 (COX-2) expression, and COX-2 inhibitio

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 p38(MAPK) and p44/42(ERK1/2) MAP kinases and cyclooxygenase-2 (COX-2) expression.

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

108 (mPGES-1) is a key enzyme that couples with cyclooxygenase-2 (COX-2) for the production of PGE(2).

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

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

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

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

113 ted through suppression of NFkappaB-mediated cyclooxygenase-2 (COX-2) in renal tubular epithelial cel

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

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

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

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

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

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

120 loped a series of anticancer agents based on cyclooxygenase-2 (COX-2) inhibitor nimesulide as a lead

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

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

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

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

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

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

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

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

129 Neuronal expression of cyclooxygenase-2 (COX-2) is enhanced by synaptic NMDARs,

130 Cyclooxygenase-2 (COX-2) is overexpressed in many human

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

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

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

134 AG-mediated IL-2 suppression is dependent on cyclooxygenase-2 (COX-2) metabolism and peroxisome proli

135 -1beta mRNA; BLP was more potent in inducing cyclooxygenase-2 (COX-2) mRNA and protein expression.

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

137 epidermal growth factor receptor 2 positive, cyclooxygenase-2 (COX-2) negative, and COX-2 positive.

138 he oxygenation of arachidonic acid by either cyclooxygenase-2 (COX-2) or 5-lipoxygenase (5-LOX), resp

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

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

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

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

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

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

145 that PGE2, one of the final products of the cyclooxygenase-2 (COX-2) pathway, can induce the mRNA ex

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

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

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

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

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

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

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

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

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

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

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

157 Cyclooxygenase-2 (COX-2), a source of inflammatory media

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

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

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

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

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

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

164 Conversely, cyclooxygenase-2 (COX-2), angiopoietin-2 (Ang-2), and pe

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

166 Genes under the control of the cyclooxygenase-2 (Cox-2), human epidermal growth factor

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

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

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

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

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

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

173 was shown to be susceptible to oxidation by cyclooxygenase-2 (COX-2).

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

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

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

177 a, while celecoxib (a selective inhibitor of cyclooxygenase 2 [COX-2]) produced moderate antihyperalg

178 Cyclooxygenase 2 (Cox2) and mammalian target of rapamyci

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

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

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

182 loop between prostaglandin E(2) (PGE(2)) and cyclooxygenase 2 (COX2), the key regulator of PGE(2) syn

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

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

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

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

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

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

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

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

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

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

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

194 Cyclooxygenase-2-derived prostaglandin E(2) (PGE(2)) is

195 set of BP responses (chemokines, cytokines, cyclooxygenase 2) differed in two respects; DMBA respons

196 Inhibition of the thromboxane receptor or cyclooxygenase-2 dramatically attenuated HOG-LDL-induced

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

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

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

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

201 Increased cyclooxygenase-2 expression and prostaglandin E2 release

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

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

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

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

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

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

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

209 lammatory cytokine and chemokine production, cyclooxygenase-2 expression, and prostaglandin E(2) prod

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

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

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

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

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

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

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

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

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

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

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

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

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

223 tly higher induction of TNF-alpha, IL-6, and cyclooxygenase-2 in J774 macrophage-like cells in respon

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

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

226 -1 beta, inducible nitric oxide synthase and cyclooxygenase-2 in the cortex after spreading depolariz

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

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

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

230 und attenuated inflammatory gene expression (cyclooxygenase-2, inducible nitric-oxide synthase, and T

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

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

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

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

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

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

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

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

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

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

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

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

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

244 Treatment with a cyclooxygenase 2 inhibitor celecoxib significantly impro

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

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

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

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

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

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

251 Cyclooxygenase-2 inhibitors (coxibs) are characterized b

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

253 ing other agents with NSAID-like mechanisms (cyclooxygenase-2 inhibitors and salicylates).

254 roidal anti-inflammatory drugs and selective cyclooxygenase-2 inhibitors that block prostanoid synthe

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

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

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

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

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

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

261 Cyclooxygenase-2 is expressed in the renal medulla where

262 o an inflammatory response, we asked whether cyclooxygenase-2, its derivative prostaglandin E2, prost

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

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

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

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

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

270 probably resulted from a large induction of cyclooxygenase 2 mRNA and protein.

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

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

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

278 both protein and messenger RNA expression of cyclooxygenase-2, prostaglandin E2, prostanoid receptor-

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

280 arks of OA, as evidenced by the induction of cyclooxygenase-2, prostaglandins (PGs), and interleukin-

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 ely to cause hypertension or thrombosis than cyclooxygenase-2-selective inhibition or deletion in viv

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

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

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

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