ライフサイエンスコーパス: COX inhibitor

1 ive COX-2 inhibitor) and indomethacin (a pan-COX inhibitor).

2 profen (800 mg 3 times a day), a nonspecific COX inhibitor.

3 or of COX-2, with diclofenac, a non-specific COX inhibitor.

4 by treatment with sulindac sulfide, a known COX inhibitor.

5 vity in this example of a diaryl-heterocycle COX inhibitor.

6 e experiments does not involve its role as a COX inhibitor.

7 or cells may be a direct target of action by COX inhibitors.

8 ltured ex vivo with or without IL-1 beta and COX inhibitors.

9 or to intracellular Ca(2+) were inhibited by COX inhibitors.

10 PGE2 should prove useful for identifying new COX inhibitors.

11 were more potent growth inhibitors than the COX inhibitors.

12 s 11-dehydro metabolite are depressed by the COX inhibitors.

13 ould be optimized by the further addition of COX inhibitors.

14 e-line prostanoid synthesis and responses to COX inhibitors.

15 ulating PGHS-2 activity and its responses to COX inhibitors.

16 effects typically associated with the use of COX inhibitors.

17 re enhanced by prostaglandins and reduced by COX inhibitors.

18 and PGE2 production and their regulation by COX inhibitors.

19 nary NO(x) and PGE(2) were corrected by both COX inhibitors.

20 activity, was added simultaneously with the COX inhibitors.

21 ed mode-of-action such as PPARa agonists and COX inhibitors.

22 f a NO donor with those of a cyclooxygenase (COX) inhibitor.

23 an macrophages compared with cyclooxygenase (COX) inhibitors.

24 nd evaluation of 18F-labeled cyclooxygenase (COX) inhibitors.

25 ry reactions to nonselective cyclooxygenase (COX) inhibitors.

26 Unlike the selective COX inhibitors 1-[(4-methylsulfonyl)phenyl]-3-trifluorom

27 Using COX inhibitors, a sequential increase of posttransplanta

28 o increase Ecat activity; and (c) allosteric COX inhibitors act by preventing FA binding to Eallo and

29 mode by analyzing the action of a series of COX inhibitors against site-directed mutants of COX-2 be

30 Although neither estradiol nor the COX inhibitors alone had an effect on PGD2 serum levels,

31 Pretreatment of tumor cells with COX inhibitors also reduces metastatic success, indicati

32 d TNF-alpha production, whereas experimental COX inhibitors and antipyretics used during human malari

33 Thus, a major effect of COX inhibitors and COX-deficiency is the induction of ke

34 on previously shown in the mice treated with COX inhibitors and in COX-deficient mice and suggest tha

35 Hence, concomitant therapy with COX inhibitors and/or IL-6R antibodies might increase th

36 Experiments using specific cyclooxygenase (COX) inhibitors and genetic knockdown approaches indicat

37 a baicalensis), indomethacin (a nonselective COX inhibitor), and celecoxib (a selective COX-2 inhibit

38 tudy we found that both piroxicam, a general COX inhibitor, and NS-398, a COX-2 selective inhibitor,

39 ty compared with rofecoxib, the nonselective COX inhibitors, and control animals.

40 (2) inhibited MMP-1, reversed the effects of COX inhibitors, and inhibited ERK activation, suggesting

41 e for testing potential benefits from common COX inhibitors as a part of AML treatments.

42 disease processes and the widespread use of COX inhibitors as therapeutic agents.

43 (NS398) and nonselective (sulindac sulfide) COX inhibitors, as well as 5-fluorouracil (5-FU), induce

44 prevented this effect, and the non-specific COX inhibitor aspirin (1 mM) also alleviated the damage.

45 each at 60 s intervals) before and after the COX inhibitor aspirin (600 mg p.o.).

46 Developmental exposure to the COX inhibitor aspirin results in mild impairment of sexu

47 celecoxib or rofecoxib, and the nonspecific COX inhibitors, aspirin, naproxen, ibuprofen, or indomet

48 Pretreatment with ibuprofen, a nonspecific COX inhibitor, attenuated the febrile and systemic respo

49 tment of bFGF- or VEGF-stimulated HMECs with COX inhibitors blocked tubular formation by about 50% to

50 -specific inhibitor, and indomethacin, a pan-COX inhibitor, but not by SC-560, a COX-1-specific inhib

51 lly treated with opioids and cyclooxygenase (COX) inhibitors, but both are limited by side effects.

52 ase from FLSCs via inhibition of ERK, and 3) COX inhibitors, by attenuating PGE inhibition of ERK, en

53 Although COX inhibitors can be used to close the PDA by lowering

54 All of the COX inhibitors caused dose-dependent decreases in IL-1be

55 Crystallographic analysis of selective COX inhibitors complexed with either isoform provides so

56 Our data indicate that COX inhibitor coprescription among aspirin users is freq

57 nducing eradication of tumors, implying that COX inhibitors could be useful adjuvants for immune-base

58 Identification of genes regulated by COX inhibitors could lead to a better understanding of t

59 this study was to analyze if cyclooxygenase (COX) inhibitors could improve the early posttransplant o

60 Cyclooxygenase (COX) inhibitors decrease tumor multiplicity in the Min m

61 Studies in COX-deficient cells and using COX inhibitors demonstrated that COX-2 mediated the high

62 e FAs can potentiate or attenuate actions of COX inhibitors depending on the FA and whether the inhib

63 In contrast, the slow, time-dependent COX inhibitors (diclofenac, indomethacin, and flurbiprof

64 cations included coculture plus or minus the COX-inhibitor, Diclofenac, or synthetic PGE(2) in the ab

65 oncentrations of salicylate, while selective Cox inhibitors did not inhibit angiogenesis in this assa

66 Ibuprofen, a structurally dissimilar COX inhibitor, did not activate Slo2.1.

67 5-LO knockout mice that were treated with a COX inhibitor during allergic sensitization and challeng

68 and nonsubstrate fatty acids (FAs) and some COX inhibitors (e.g. naproxen) preferentially bind to th

69 Furthermore, multiple distinct classes of COX inhibitors efficiently blocked neurite loss in prima

70 t in which the R120Q subunit cannot bind the COX inhibitor flurbiprofen, was inhibited by flurbiprofe

71 raise concern regarding the use of selective COX inhibitors for the management of preterm labor.

72 -overexpressing cells with the non-selective COX inhibitor ibuprofen (1 microM, 48 h) or with the spe

73 4-bromophenacyl bromide (4-BPB), the general COX inhibitor ibuprofen (IB), and the highly selective C

74 d significantly not only by the nonselective COX inhibitor ibuprofen but also by the COX-2 selective

75 Furthermore, the well tolerated COX inhibitor ibuprofen was protective against IL-1beta-

76 hosphonovalerate as well the cyclooxygenase (COX) inhibitor ibuprofen.

77 The inhibitory activity of rapid, reversible COX inhibitors (ibuprofen, naproxen, mefenamic acid, and

78 However, medical use of COX inhibitors in glioblastoma treatment has been limite

79 Furthermore, COX inhibitors in humans, as well as platelet depletion,

80 nimals are spared the hemorrhaging caused by COX inhibitors in the gut, where prostaglandins are inst

81 77 may represent more effective therapy than COX inhibitors in treating uveitis and ocular diseases w

82 , markedly enhanced, whereas cyclooxygenase (COX) inhibitors including aspirin, piroxicam, and NS398

83 COX inhibitors, including coxibs, nonselective nonsteroi

84 1.7 nmol OH(-) min(-1)) by the non-specific COX inhibitor indomethacin (5 mg kg(-1) I.P.).

85 tube formation by EPCs were inhibited by the COX inhibitor indomethacin or by genetic inactivation of

86 as an adjuvant and treated the mice with the COX inhibitor indomethacin or vehicle for analyses of th

87 The COX inhibitor indomethacin or vehicle was administered i

88 aglandin synthesis in newborn males with the COX inhibitor indomethacin permanently downregulates mar

89 beta-casein gene, which was inhibited by the Cox inhibitor indomethacin.

90 200 (5 mg kg(-1)) or by the cyclo-oxygenase (COX) inhibitor indomethacin (20 mg kg(-1)).

91 of coinfected mice with the cyclooxygenase (COX) inhibitor indomethacin reduces the infectious burde

92 Treatment with the COX-inhibitor indomethacin and/or the clinical monoclona

93 ly blocked in the presence of a nonselective COX inhibitor (indomethacin) or a selective COX-2 inhibi

94 Administration of a nonselective COX inhibitor (indomethacin), selective COX-1 (valeryl s

95 A non-selective COX inhibitor (indomethacin, 15 mg kg(-1) I.P.), a selec

96 (NS-398; 1 mg/kg x 7 days; N = 16), general COX inhibitor (indomethacin; 1 mg/kg x 7 days; N = 16),

97 OX-2 inhibitor, SC58238, and the nonspecific COX inhibitor, indomethacin, effectively inhibited the e

98 791, as well as the traditional nonsteroidal COX inhibitor, indomethacin.

99 atment of platelets with the cyclooxygenase (COX) inhibitor, indomethacin (20 microM), the thromboxan

100 Cyclooxygenase (COX) inhibitors, indomethacin and NS-398, did not reduce

101 tment of W256 cells with various LOX but not COX inhibitors induced apoptotic cell death, which could

102 ophils to aspirin or sodium salicylate (poor COX inhibitor) inhibited Erk activity and adhesiveness o

103 Sulindac sulfide, a COX inhibitor, inhibited the growth of non-small-cell lu

104 were associated with data indicating that a COX inhibitor is not preventive in NMBA-induced rat esop

105 t of combined therapy with aspirin and other COX inhibitors is not yet clear.

106 inflammatory drugs (NSAIDs), cyclooxygenase (COX) inhibitors, is well established, but responsible mo

107 The pan-COX inhibitor ketorolac continuously and significantly d

108 Sodium salicylate, a poor COX inhibitor, likewise enhanced IL-1-mediated COX-2 gen

109 proapoptotic protein, and its regulation by COX inhibitors may provide new clues for explaining thei

110 (PLA2) inhibitor], ibuprofen [a nonselective COX inhibitor], neomycine [a phospholipase C (PLC) inhib

111 motes CRC progression, and both nonselective COX inhibitors (NSAIDs) and selective COX-2 inhibitors (

112 tes to the proapoptotic effects of high-dose COX inhibitors (NSAIDs) by serving as a downstream media

113 We evaluated the effect of cyclooxygenase (COX) inhibitors (NSAIDs) on human colon carcinoma cells

114 o compare the activity of target ligands and COX inhibitors on PGE2 synthesis and release, the respon

115 the pharmacologic effects of specific spinal COX inhibitors on uterine cervical distention induced no

116 cific NO synthase inhibitor, a non-selective COX inhibitor or combined inhibition during perfusion of

117 Treatment with COX inhibitors or albumin restored immune competence and

118 ere exposed to low doses of the nonselective COX inhibitor piroxicam and the ornithine decarboxylase

119 th was unaffected by either the nonselective COX inhibitor piroxicam or the selective COX-2 inhibitor

120 this study, we determined the effects of the cox inhibitor, piroxicam, on tumor response, apoptotic i

121 Cyclooxygenase (COX) inhibitors, present during incubation with endotoxi

122 xplain a component of the mechanism by which COX inhibitors prevent colorectal cancer in humans.

123 s are among the most potent multitarget FAAH/COX inhibitors reported so far in the literature and thu

124 d the well-known side effects of opioids and COX inhibitors, resolvins may represent new analgesics f

125 2 production with diclofenac, a nonselective COX inhibitor, resulted in reduced tumor growth in an in

126 r reversed by addition of the nonfluorescent COX inhibitor (S)-flurbiprofen.

127 The nonselective COX inhibitors salicylate and indomethacin enhanced the

128 etylated form of aspirin), and the selective Cox inhibitors SC560 and Celecoxib on endothelial cell p

129 hough sharing a common response with AERD to COX inhibitors, seems to have a distinctive phenotype, b

130 Furthermore, COX inhibitors significantly decreased PG production.

131 First, the non-COX inhibitor, sodium salicylate, was as potent as aspir

132 ic effects than those seen with nonselective COX inhibitors such as acetylsalicylic acid (aspirin).

133 levels were increased in cells treated with COX inhibitors such as NS-398, nimesulide, SC-58125, and

134 Classical cyclooxygenase (COX) inhibitors, such as indomethacin, which inhibit bot

135 ppaB translocation inhibitor), or ibuprofen (COX inhibitor) suppressed molecular changes and inhibite

136 ts into the mechanism of negative effects of COX inhibitors that may influence the treatment of sever

137 ture of T. suis with several cyclooxygenase (COX) inhibitors that inhibit mammalian prostaglandin syn

138 We used nonselective and selective COX inhibitors to determine the role of COX on inducible

139 may be an alternative approach to the use of COX inhibitors to prevent tumor metastasis.

140 hifted focus away from these cyclooxygenase (COX) inhibitors to seek additional therapeutic targets i

141 evaluated the ability of piroxicam, a potent COX inhibitor, to prevent postinitiation events of NMBA-

142 e observed in COX-deficient keratinocytes or COX-inhibitor treated wild-type cells.

143 lpha formation is substantially depressed by COX inhibitors, urinary excretion of the compound is una

144 However, the COX inhibitors used were shown to cause relevant hepatot

145 Indomethacin, a nonselective cyclooxygenase (COX) inhibitor, was modified in three distinct regions i

146 COX inhibitors were prescribed to the majority of aspiri

147 of xenograft tumor volume when nonselective COX inhibitors were used in combination with erlotinib.

148 ation that may guide the design of dual FAAH-COX inhibitors with superior analgesic efficacy.

149 alicylic acid (aspirin) is a cyclooxygenase (COX) inhibitor, yet some of its therapeutic effects are