ライフサイエンスコーパス: sodium salicylate

1 by aspirin and indomethacin and minimally by sodium salicylate.

2 AA caused toxicity that was increased by sodium salicylate.

3 he antiinflammatory agents dexamethasone and sodium salicylate.

4 s contain cetyltrimethylammonium bromide and sodium salicylate.

5 t manner, and this increase was inhibited by sodium salicylate.

6 ts accumulation was shown to be inducible by sodium salicylate.

7 Cells were treated with sodium salicylate (10(-7)-10(-4) m) or vehicle for 30 mi

8 Sodium salicylate, a poor COX inhibitor, likewise enhanc

9 Because sodium salicylate, a related compound, modulates the hea

10 e drugs against COX-2, with the exception of sodium salicylate (A549 cells).

11 Sodium salicylate acutely (30 min) also caused a concent

12 Sodium salicylate also has antiviral effects as the resu

13 Sodium salicylate also prevented IL-1beta from inducing

14 Sodium salicylate, an inhibitor of IKK beta, but not IKK

15 Sodium salicylate and acetylsalicylic acid are drugs use

16 teroidal anti-inflammatory agents, including sodium salicylate and aspirin, can inhibit NF-kappa B-de

17 Inhibitors of NF-kappa B activity, sodium salicylate and cyclopentenone prostaglandins (pro

18 me sensitive to apoptosis in the presence of sodium salicylate and prostaglandins.

19 idonyl trifluoromethylketone, staurosporine, sodium salicylate, and C6-ceramide, were studied.

20 lumiracoxib, meloxicam, naproxen, rofecoxib, sodium salicylate, and SC560 as inhibitors of COX-1 and

21 e different salicylate-based drugs (aspirin, sodium salicylate, and sulfasalazine) on the development

22 This study demonstrates that sodium salicylate at a therapeutic concentration suppres

23 Aspirin and sodium salicylate at therapeutic concentrations equipote

24 Elucidation of the mechanism whereby sodium salicylate blocks TNF-induced p42/p44 MAPK activa

25 the antiinflammatory effects of aspirin and sodium salicylate, but not glucocorticoids, are largely

26 ently, we demonstrated that both aspirin and sodium salicylate, but not indomethacin, inhibited the a

27 ome inhibitor ALLN, the antioxidant PDTC, or sodium salicylate, but not the glucocorticoid dexamethas

28 Whether aspirin and sodium salicylate could reduce invasiveness and whether

29 ALLN, PDTC, or sodium salicylate decreased P-selectin expression withou

30 The effect of a single i.p. injection of sodium salicylate depended on the initial power of the e

31 ta-HSD1-deficient mice and C57Bl/6 mice with sodium salicylate for 4 weeks.

32 expression, whereas ethylene, abscisic acid, sodium salicylate, fusicoccin, or beta-aminobutyric acid

33 In contrast, both mesalamine and sodium salicylate have been shown to lower the thermal i

34 nflammatory drug aspirin and its metabolite, sodium salicylate, have profound effects on cellular pro

35 Aspirin and its major metabolite sodium salicylate induced apoptosis and decreased colon

36 pathetic stress via the locus coeruleus; [3] sodium salicylate induces an acute excitotoxicity by pot

37 Furthermore, by reducing ROS, aspirin and sodium salicylate inhibit CMV-induced NFkappaB activatio

38 We found that sodium salicylate inhibited activation of NF-kappa B (p5

39 Sodium salicylate inhibited cytokine-induced nitrite acc

40 Treatment with aspirin or sodium salicylate inhibited invasiveness of the LMP1-exp

41 Sodium salicylate inhibited prostaglandin E2 release whe

42 reatment of endothelial cell monolayers with sodium salicylate inhibited transendothelial migration o

43 The mechanism of aspirin and sodium salicylate inhibition is due to binding of these

44 Sodium salicylate inhibits activation of the transcripti

45 ectromobility shift assays demonstrated that sodium salicylate inhibits IL-1beta-induced nuclear fact

46 icate that the sites of action through which sodium salicylate inhibits these negative effects of IL-

47 Thus, sodium salicylate is an effective inhibitor of COX-2 act

48 amine possible sites of action through which sodium salicylate might affect IL-1beta/PGE(2) interacti

49 armacological concentrations (1 to 3 mmol/L) sodium salicylate (Na-Sal) can potently induce programme

50 Sodium salicylate (NaSal) and other nonsteroidal anti-in

51 Sodium salicylate (NaSal) can block NF-kappaB activation

52 The nonsteroidal anti-inflammatory drug sodium salicylate (NaSal) interferes with TNF-induced NF

53 In a previous study, we demonstrated that sodium salicylate (NaSal) selectively inhibits tumor nec

54 Sodium salicylate (NaSal) treatment induced apoptotic ce

55 the soxRS system, and to the weak acid salt sodium salicylate (NaSal), an inducer of the marRA syste

56 In this report, the effects of aspirin and sodium salicylate on COX-2 expressions in human umbilica

57 ls in culture to the anti-inflammatory drugs sodium salicylate or indomethacin results in activation

58 In this study, it was demonstrated that sodium salicylate, plumbagin, 2, 4-dinitrophenol, and me

59 Exposure of neutrophils to aspirin or sodium salicylate (poor COX inhibitor) inhibited Erk act

60 In addition, the anti-inflammatory drug sodium salicylate, previously demonstrated to inhibit NF

61 In the JB6 cell culture system, aspirin or sodium salicylate (SA) inhibited UVB-induced AP-1 activi

62 Aspirin and sodium salicylate (salicylates) have been reported to ha

63 hat the anti-inflammatory agents aspirin and sodium salicylate specifically inhibit IKK-beta activity

64 ubunits other than RelA, we used aspirin and sodium salicylate to inhibit kinases that activate NF-ka

65 te, as well as succinylcholine chloride with sodium salicylate using acetone as a neutral marker, are

66 arachidonic acid was increased to 30 microM, sodium salicylate was a very weak inhibitor of COX-2 act

67 The inhibitory effect of sodium salicylate was restricted to serum-deprived quies

68 ation between AERD and control subjects, and sodium salicylate was without effect.

69 First, the non-COX inhibitor, sodium salicylate, was as potent as aspirin in inhibitin

70 the antiinflammatory effects of aspirin and sodium salicylate were independent of the levels of pros

71 nd responds to phenolic compounds, including sodium salicylate, which inhibit its activity.