ライフサイエンスコーパス: cyclo-oxygenase

1 ory actions to effects on oxidation state of cyclo-oxygenase.

2 ng terminals, but resistant to inhibition of cyclo-oxygenases.

3 man vessels and endothelial cells containing cyclo-oxygenase-1 (COX-1) without any detectable COX-2,

4 hacin or diclofenac, which also inhibit both cyclo-oxygenase-1 and cyclo-oxygenase-2, were unaffected

5 2 selective inhibitor rofecoxib or the mixed cyclo-oxygenase-1/cyclo-oxygenase-2 inhibitors ibuprofen

6 ts the inducible isoform of cyclo-oxygenase, cyclo-oxygenase 2 (COX-2).

7 Cyclo-oxygenase 2 (COX2), an inducible isoform of prosta

8 Methylation status of the p14, p16, cyclo-oxygenase 2 (COX2), O(6)-methyl-guanine methyltran

9 Cyclo-oxygenase 2 (COX2)-selective inhibitors should red

10 The potential for cyclo-oxygenase 2 (COX2)-selective inhibitors to increas

11 OCS-3]) and mediators of energy expenditure (cyclo-oxygenase 2 [COX-2]), we studied the effect of CNT

12 appaBalpha and proinflammatory genes such as cyclo-oxygenase 2 and interleukin 8.

13 Non-selective and selective cyclo-oxygenase 2 inhibitors have preliminary data from

14 a-2 agonists, beta-blockers,corticosteroids, cyclo-oxygenase 2 inhibitors, and regional anesthetic bl

15 A search for chemoprevention agents, such as cyclo-oxygenase 2 inhibitors, as well as for putative en

16 Current exposure to cyclo-oxygenase 2 selective and non-selective NSAIDs was

17 including overexpression of IL-6, IL-1beta, cyclo-oxygenase 2, M-CSF, and IDO.

18 nducible NO synthase, arginase-1, TNF-alpha, cyclo-oxygenase 2, vascular endothelial growth factor [V

19 ripts of a limited number of genes including cyclo-oxygenase-2 (COX-2) and major histocompatibility c

20 Prostanoids produced via the action of cyclo-oxygenase-2 (COX-2) appear central to many inflamm

21 ates parathyroid-related peptide (PTHrP) and cyclo-oxygenase-2 (COX-2) as possible factors underlying

22 ophosphatidic acid (LPA) lead to synergistic cyclo-oxygenase-2 (COX-2) expression, an enzyme strongly

23 e, mutagenesis, apoptosis, angiogenesis, and cyclo-oxygenase-2 (COX-2) expression.

24 inhibits nitric-oxide synthase-2 (NOS-2) and cyclo-oxygenase-2 (COX-2) expressions in RAW 264.7 stimu

25 -2), matrix metalloproteinase-9 (MMP-9), and cyclo-oxygenase-2 (COX-2) in the mammary gland.

26 dies suggest that treatment with a selective cyclo-oxygenase-2 (COX-2) inhibitor may augment the anti

27 Cyclo-oxygenase-2 (COX-2) selective inhibitors have been

28 of interleukin-8 (IL-8), IL-6, IL-1beta, and cyclo-oxygenase-2 (COX-2) were greatest in differentiate

29 Cyclo-oxygenase-2 (COX-2), a rate-limiting enzyme for pr

30 Cyclo-oxygenase-2 (COX-2), an inducible enzyme important

31 SAIDs), particularly selective inhibitors of cyclo-oxygenase-2 (COX-2), is associated with an increas

32 expression of the pro-inflammatory mediator cyclo-oxygenase-2 (COX-2), providing a mechanism whereby

33 s, such as inflammatory responses, including cyclo-oxygenase-2 (Cox-2).

34 We have demonstrated previously that cyclo-oxygenase-2 (COX2), the rate-limiting enzyme in th

35 Here, we have used an in vitro model of cyclo-oxygenase-2 activity (A549 cells stimulated with I

36 uated by inhibiting the prostanoid mediators cyclo-oxygenase-2 and 5-lipoxygenase and CC chemokine re

37 tivity, and (iii) protein expression of ODC, cyclo-oxygenase-2 and nitric oxide synthase.

38 t of titres of lentiviral vectors expressing Cyclo-oxygenase-2 by 600-fold, and adenoviral vectors ex

39 Selective inhibition of cyclo-oxygenase-2 has been associated with an increased

40 over nonsteroidal anti-inflammatory drug and cyclo-oxygenase-2 inhibitor safety continues.

41 ked current also was blocked by the specific cyclo-oxygenase-2 inhibitor SC-236.

42 following treatment with NS-398, a selective cyclo-oxygenase-2 inhibitor was evaluated.

43 sessed the effect of 3-year treatment with a cyclo-oxygenase-2 inhibitor, rofecoxib (25 mg), on recur

44 tor rofecoxib or the mixed cyclo-oxygenase-1/cyclo-oxygenase-2 inhibitors ibuprofen and naproxen were

45 ear has led to a reassessment of the role of cyclo-oxygenase-2 inhibitors in osteoarthritis therapy a

46 c pain is typically treated with opioids and cyclo-oxygenase-2 inhibitors with well known side effect

47 of nonsteroidal anti-inflammatory drugs and cyclo-oxygenase-2 inhibitors.

48 resulted in specific induction of Bcl-2 and cyclo-oxygenase-2 proteins, both of which are thought to

49 Similarly the inhibitory effects of the cyclo-oxygenase-2 selective inhibitor rofecoxib or the m

50 some NSAIDs, including the newly introduced cyclo-oxygenase-2 selective inhibitor rofecoxib, owe par

51 Cyclo-oxygenase-2 selective inhibitors and non-selective

52 s of nonsteroidal anti-inflammatory drug and cyclo-oxygenase-2 therapy for individuals is covered.

53 Cyclo-oxygenase-2(-/-) mice had increased plasma levels

54 okeratin, high-molecular-weight cytokeratin, cyclo-oxygenase-2, EMA, HER2, matrix metalloproteinases

55 such as inducible nitric oxide synthase and cyclo-oxygenase-2, reduce ischemic damage with an extend

56 hich also inhibit both cyclo-oxygenase-1 and cyclo-oxygenase-2, were unaffected by t-butylOOH.

57 ious impact that select therapies (including cyclo-oxygenase-2-specific inhibitors) may have in terms

58 These observations dispel the notion that cyclo-oxygenase-3 is involved in the actions of acetamin

59 inhibits a distinct form of cyclo-oxygenase, cyclo-oxygenase-3.

60 sm that is, at least in part, independent of cyclo-oxygenase activation.

61 , alternatively, the restoration of PTHrP or cyclo-oxygenase activity by the administration of PTH an

62 t acetaminophen is an effective inhibitor of cyclo-oxygenase activity in intact cells.

63 ise mechanism of action for acetaminophen on cyclo-oxygenase activity is debated.

64 +/- 54.9 % of control following blockade of cyclo-oxygenase activity with naproxen (10 microM).

65 g of free radicals, or by inhibition of both cyclo-oxygenase and lipoxygenase in combination.

66 se of arachidonic acid, which is acted on by cyclo-oxygenase and lipoxygenase resulting in the format

67 e to ANG II depends largely on activation of cyclo-oxygenase and production of prostaglandins.

68 Aspirin, a nonselective COX-1 (cyclo-oxygenase) and COX-2 inhibitor may result in gastr

69 ytokines, and suppresses phospholipase A(2), cyclo-oxygenase, and nitric oxide synthase.

70 e caused by the previous suggested effect on cyclo-oxygenase, as inhibition also was observed in the

71 ophen has no affinity for the active site of cyclo-oxygenase but instead blocks activity by reducing

72 xide synthase, soluble guanylate cyclase and cyclo-oxygenase but was blocked by 25 mm potassium.

73 (200 microg/5 microl aCSF), an inhibitor of cyclo-oxygenase, but not with losartan (25 microg/5 micr

74 Should selective cyclo-oxygenase (COX) 2 inhibitors be used?

75 and whether its effects are mediated through cyclo-oxygenase (COX) and prostaglandins (PG).

76 inhibition of prostaglandin synthesis via a cyclo-oxygenase (COX) enzyme was central to both the the

77 The role of different isoforms of cyclo-oxygenase (COX) in mediating the acute (0-6 h) and

78 g(-1)) and SB-222200 (5 mg kg(-1)) or by the cyclo-oxygenase (COX) inhibitor indomethacin (20 mg kg(-

79 the stomach, production of prostaglandins by cyclo-oxygenase (COX) is believed to be important in muc

80 Metabolism of arachidonic acid by the cyclo-oxygenase (COX) pathway generates a family of pros

81 ed vasodilatation with nitric oxide (NO) and cyclo-oxygenase (COX) signalling pathways, microdialysis

82 Cyclo-oxygenase (COX), the enzyme responsible for conver

83 of NSAIDs is their inhibition of the enzyme cyclo-oxygenase (COX), which catalyses the synthesis of

84 dal anti-inflammatory drugs (NSAIDs) inhibit cyclo-oxygenase (COX), which leads to suppression of COX

85 ighly-sensitive assay, and on serum platelet-cyclo-oxygenase (COX)-1-derived thromboxane (Tx) B2 conc

86 prostacyclin (PGI2) derived from adenoviral cyclo-oxygenase (COX)-1/prostacyclin synthase (PGIS) (Ad

87 Cyclo-oxygenase (COX)-2 selective inhibitors decrease up

88 Upper gastrointestinal safety of cyclo-oxygenase (COX)-2 selective inhibitors versus trad

89 (NSAID) can be associated with inhibition of cyclo-oxygenase (COX)-2 whereas their harmful side effec

90 ed rapid expression of interleukin-15, CD83, cyclo-oxygenase (COX)-2, and CD25 by CD3- cells (p=0.005

91 ction of aspirin is inhibition of the enzyme cyclo-oxygenase (COX).

92 inhibition of nitric oxide (NO) synthase or cyclo-oxygenase (COX).

93 Increased generation of cyclo-oxygenase (COX-1 and COX-2)-derived vasoconstricto

94 interaction between PPARgamma and inducible cyclo-oxygenase (COX-2) in rat aortic vascular smooth mu

95 of nitric oxide synthase (NOS; with l-NAME), cyclo-oxygenase (COX; with indomethacin) and endothelium

96 a 1-week high-salt (HS) diet on the role of cyclo-oxygenases (COX-1 and COX-2) and the vasoconstrict

97 selectively targets the inducible isoform of cyclo-oxygenase, cyclo-oxygenase 2 (COX-2).

98 phen selectively inhibits a distinct form of cyclo-oxygenase, cyclo-oxygenase-3.

99 In addition, nitric oxide and cyclo-oxygenase-derived byproducts are required for full

100 extent of I(CRAC), whereas inhibition of the cyclo-oxygenase enzymes was without effect.

101 ic responses, such as inducible NO synthase, cyclo-oxygenase II, and collagenase.

102 l effective in the presence of inhibitors of cyclo-oxygenase (indomethacin, 10 microM), lipoxygenase

103 shes bombesin-induced gastroprotection while cyclo-oxygenase inhibition partially reverses this effec

104 .v.) and NPC-17731 (40 micrograms kg-1 i.v., cyclo-oxygenase inhibition with indomethacin (5 mg kg-1

105 d reduced ET-induced vascular leakage with a cyclo-oxygenase inhibitor (indomethacin), agents that in

106 t influenced by pretreatment with either the cyclo-oxygenase inhibitor indomethacin or the leukotrien

107 gene expression in T cells, whereas the weak cyclo-oxygenase inhibitor salicylic acid was at least as

108 yet, undeveloped therapeutic window for the "cyclo-oxygenase inhibitor".

109 ed in the presence of high concentrations of cyclo-oxygenase inhibitor, aspirin.

110 The development of selective cyclo-oxygenase inhibitors (COX-II) and confirmation of

111 administration of indomethacin or celecoxib (cyclo-oxygenase inhibitors), pyrilamine, aprepitant (a n

112 omethacin, suggesting that the activation of cyclo-oxygenase is not involved.

113 tested are physiological substrates for the cyclo-oxygenase, lipoxygenase and epoxygenase pathways,

114 esting that AA did not exert its effects via cyclo-oxygenase, lipoxygenase or cytochrome P-450 (cP-45

115 ibition of Kv4 channels was not prevented by cyclo-oxygenase, lipoxygenase, or cytochrome P-450 inhib

116 do), an inhibitor of the metabolism of AA by cyclo-oxygenase, nor nordihydroguaiaretic acid (NDGA), a

117 ls, and is independent of the release of NO, cyclo-oxygenase or cytochrome P450 products.

118 ce for metabolism of arachidonic acid by the cyclo-oxygenase pathway.

119 e afferents appears to be independent of the cyclo-oxygenase pathway.

120 and substrate supply, and not the isoform of cyclo-oxygenase present, dictate the effects of NSAIDs o

121 Increased production of bradykinin (BK) and cyclo-oxygenase products (i.e. prostaglandins (PGs)) occ

122 Acetaminophen works by lowering cyclo-oxygenase products preferentially in the central n

123 of endothelin and possibly vasoconstrictive cyclo-oxygenase products.

124 micro g/5 micro l, i.c.v.), an inhibitor of cyclo-oxygenase, showing that they are mediated by prost

125 (200 microg/5 microl; icv), an inhibitor of cyclo-oxygenase, significantly attenuated the ANG II-ind

126 , unco-ordinated-5H3 (unc5H3), doublecortin, cyclo-oxygenase, sonic hedgehog and Disrupted in schizop

127 vity by reducing the active oxidized form of cyclo-oxygenase to an inactive form.

128 Inhibition of cyclo-oxygenase with naproxen (10 microM) prevented sens