ライフサイエンスコーパス: N-acetylpenicillamine

1 es and incubated with the NO donor S-nitroso-N-acetylpenicillamine.

2 relaxation induced by the NO donor S-nitroso-N-acetylpenicillamine.

3 ed by the addition of the NO donor S-nitroso-N-acetylpenicillamine.

4 itions with the nitric oxide donor S-nitroso-N-acetylpenicillamine.

5 S-Nitroso-N-acetylpenicillamine, a compound that liberates nitric

6 s was inhibited by the addition of S-nitroso-N-acetylpenicillamine, a nitric oxide (NO)-generating co

7 Addition of S-nitroso-N-acetylpenicillamine, a nitric oxide donor, prevented V

8 s M1 macrophage polarization while S-nitroso-N-acetylpenicillamine, a NO donor, suppresses M1 macroph

9 O donors, sodium nitroprusside and S-nitroso-N-acetylpenicillamine, alone did not increase basal PGE2

10 NOC-18), S-nitrosoglutathione, and S-nitroso-N-acetylpenicillamine also suppressed CYP2B proteins.

11 dy Jo2, a nitric oxide (NO) donor (S-nitroso-N-acetylpenicillamine), an NO inhibitor (N(G)-methyl-L-a

12 h those of the nitric oxide donor, S-nitroso-N-acetylpenicillamine, an agent we showed previously to

13 onse, the vasodilation elicited by S-nitroso-N-acetylpenicillamine, an NO donor that activates cGMP s

14 slices to the nitric oxide donors, S-nitroso-N-acetylpenicillamine and S-nitroso-glutathione, reveale

15 Using the NO releasing agents S-nitroso-N-acetylpenicillamine and sodium nitroprusside it was de

16 ated with the nitric oxide donors, S-nitroso-N-acetylpenicillamine and sodium nitroprusside, or the s

17 ever, treatment with the NO donors S-nitroso-N-acetylpenicillamine and spermine NONOate [N-(-aminoeth

18 y NO donors, sodium nitroprusside, S-nitroso-N-acetylpenicillamine, and S-nitrosoglutathione, and H2O

19 ionomycin, the nitric oxide donor S-nitroso-N-acetylpenicillamine, and the protein kinase G activato

20 imilarly, sodium nitroprusside and S-nitroso-N-acetylpenicillamine by themselves did not induce mRNA

21 y the addition of 400 microM SNAP (S-nitroso-N-acetylpenicillamine) caused a 10-fold increase in hboN

22 sside inhibited HIV-PR by 70%, and S-nitroso-N-acetylpenicillamine completely inhibited the enzyme.

23 The NO donor S-nitroso-N-acetylpenicillamine decreased dialysate GABA at a 500

24 The NO donor S-nitroso-N-acetylpenicillamine decreases ceramide-induced vWF rel

25 ly, treatment of EC with NO donor, S-nitroso-N-acetylpenicillamine, did not activate SREBP, suggestin

26 Moreover, S-nitrosoglutathione and S-nitroso-N-acetylpenicillamine directly blocked the activity of r

27 We found that the NO donor S-nitroso-N-acetylpenicillamine failed to block DNA synthesis in S

28 -nitro-6-methoxy-3-hexeneamide and S-nitroso-N-acetylpenicillamine greatly enhanced the formation of

29 OS-7 cells, the nitric oxide donor S-nitroso-N-acetylpenicillamine increased the activity of wild-typ

30 S-nitroso-N-acetylpenicillamine inhibited Bid cleavage, the mitoch

31 NO donors S-nitrosoglutathione and S-nitroso-N-acetylpenicillamine mimicked CYP2B1 protein suppressio

32 S-nitroso-N-acetylpenicillamine or (Z)-1-[N-(2-aminoethyl)-N-(2-am

33 exposed to an exogenous NO donor, S-nitroso-N-acetylpenicillamine or a substrate inhibitor of NO syn

34 neuroblastoma cells with NO donors S-nitroso-N-acetylpenicillamine or sodium nitroprusside in vitro b

35 the addition of NO donor molecules S-nitroso-N-acetylpenicillamine or sodium nitroprusside to VSMC do

36 r, in which the nitric oxide donor S-nitroso-N-acetylpenicillamine reduces urea transporter-A reporte

37 asing levels of nitric oxide using S-nitroso-N-acetylpenicillamine resulted in a decrease in cell inv

38 t sensitization whereas NO donors (S-nitroso-N-acetylpenicillamine) sensitized these cells to TNF-alp

39 We report that 2 NO donors, S-nitroso-N-acetylpenicillamine (SNAP) and 2, 2-(hydroxynitrosohyd

40 and endogenous sources of NO, from S-nitroso-N-acetylpenicillamine (SNAP) and bradykinin or carbachol

41 vating agents such as the NO donor S-nitroso-N-acetylpenicillamine (SNAP) and C-type natriuretic pept

42 ylated in response to the NO donor S-nitroso-N-acetylpenicillamine (SNAP) and the activation was rapi

43 Exposure to the NO donor (+/-)-s-nitroso-n-acetylpenicillamine (SNAP) blocked increases in lamini

44 nds sodium nitroprusside (SNP) and S-nitroso-N-acetylpenicillamine (SNAP) both inhibited the DNA bind

45 er (100-500 mum), concentration of S-nitroso-N-acetylpenicillamine (SNAP) can reverse the effect of l

46 The NO donor S-nitroso-N-acetylpenicillamine (SNAP) induced apoptosis without i

47 rat hepatocytes with the NO donor S-nitroso-N-acetylpenicillamine (SNAP) induced the expression of h

48 As a consequence, the NO donor S-nitroso-N-acetylpenicillamine (SNAP) inhibits lipopolysaccharide

49 ors sodium nitroprusside (SNP) and S-nitroso-N-acetylpenicillamine (SNAP) on cell cycle activity in V

50 s of authentic NO and the NO donor S-nitroso-N-acetylpenicillamine (SNAP) on swelling-activated chlor

51 (SNP), S-nitroglutathione (GSNO), S-nitroso-N-acetylpenicillamine (SNAP) or 3-morpholinosydnonimine

52 n culture to the nitrovasodilators S-nitroso-N-acetylpenicillamine (SNAP) or sodium nitroprusside (SN

53 eration of ONOO- with the NO donor S-nitroso-N-acetylpenicillamine (SNAP) plus the superoxide-releasi

54 , S-nitrosoglutathione (GSNO), and S-nitroso-N-acetylpenicillamine (SNAP) reversibly oxidized recombi

55 odilation elicited by the NO donor S-nitroso-N-acetylpenicillamine (SNAP) was inhibited by ODQ and TE

56 d nitrite levels at 24 h caused by S-nitroso-N-acetylpenicillamine (SNAP), a direct nitric oxide (NO)

57 sol isolated from hepatocytes with S-nitroso-N-acetylpenicillamine (SNAP), a nitric oxide donor, resu

58 hate (8-Br-cGMP), a cGMP analog or S-nitroso-N-acetylpenicillamine (SNAP), a NO donor essentially shu

59 used: spermine NONOate (SP), (+/-)-S-nitroso-N-acetylpenicillamine (SNAP), and S-nitrosoglutathione (

60 nducible NOS KO mice, the NO donor S-nitroso-N-acetylpenicillamine (SNAP), and the NOS inhibitor N-im

61 with the nitric oxide (NO) donor, S-nitroso-N-acetylpenicillamine (SNAP), and the phosphodiesterase

62 The NO donor S-nitroso-N-acetylpenicillamine (SNAP), at all concentrations, sup

63 iethylenetriamine/NO (DETA/NO) and S-nitroso-N-acetylpenicillamine (SNAP), at doses previously shown

64 Three such agents, S-nitroso-N-acetylpenicillamine (SNAP), diethylenetriamine NO addu

65 -nitroglutathione (GSNO) and (+/-)-S-nitroso-N-acetylpenicillamine (SNAP), directly inhibited macroph

66 Ns) by treatment with the NO donor S-nitroso-N-acetylpenicillamine (SNAP), for short (6 h) or prolong

67 incubated with NO or the NO donor, S-nitroso-N-acetylpenicillamine (SNAP), indicate a rapid loss of t

68 using the NO.-generating compound S-nitroso-N-acetylpenicillamine (SNAP), or by stimulating cells wi

69 An NO donor, S-nitroso-N-acetylpenicillamine (SNAP), suppressed apoptosis of NK

70 ced TH17 cell differentiation, and S-nitroso-N-acetylpenicillamine (SNAP), the NO donor, dosedependen

71 itric oxide (NO), and the NO donor S-nitroso-N-acetylpenicillamine (SNAP), which circumvent plasma me

72 the spontaneous nitric oxide donor S-nitroso-N-acetylpenicillamine (SNAP).

73 with sodium nitroprusside (SNP) or S-nitroso-N-acetylpenicillamine (SNAP).

74 ther 8-Br-PET-cGMP or the NO donor S-nitroso-N-acetylpenicillamine (SNAP).

75 oscillations were also evoked with S-nitroso-N-acetylpenicillamine (SNAP, 1 microM).

76 addition of an exogenous NO donor, S-nitroso-N-acetylpenicillamine (SNAP, 10(-8) M) or an analog of c

77 high concentration of the NO donor S-nitroso-N-acetylpenicillamine (SNAP, 100 micromol/L) significant

78 i.v., 4 times [group II, n=5]) or S-nitroso-N-acetylpenicillamine (SNAP, 2.5 microg x kg(-1) x min(-

79 The RSNO compounds we used were S-nitroso-N-acetylpenicillamine (SNAP, 5 to 10 nmol/L or 100 to 80

80 S-nitroso-N-acetylpenicillamine (SNAP, 9 +/- 3% to 50 +/- 8%), bra

81 S-Nitroso-N-acetylpenicillamine (SNAP; 10 microM), an NO donor, re

82 0K) during suffusion with vehicle, S-nitroso-N-acetylpenicillamine (SNAP; 100 microM) and 3-morpholin

83 In the resting state, NO donors S-nitroso-N-acetylpenicillamine (SNAP; 50 microM) and sodium nitro

84 I; 1 mM) or the nitric oxide donor S-nitroso-N-acetylpenicillamine (SNAP; 500 microM-5 mM) were studi

85 y cultured RCECs with an NO donor, S-nitroso-N-acetylpenicillamine (SNAP; N-acetyl-3-(nitrosothio)-D-

86 eated with or without the NO donor 3-nitroso-N:-acetylpenicillamine (SNAP) and the expression of x(c)

87 osed to combinations of NO donors (S-nitroso-N-acetylpenicillamine [SNAP] and others), a cGMP analogu

88 ol donors S-nitrosoglutathione and S-nitroso-N-acetylpenicillamine suppressed caspase-9 and caspase-3

89 When FLS were cultured with S-nitroso-N-acetylpenicillamine, the pattern of MMR expression in

90 Through the use of S-nitroso-N-acetylpenicillamine, which releases NO upon exposure t

91 S-nitroso-N-acetylpenicillamine, (Z)-1-[N-(2-aminoethyl)-N-(2-amin