ライフサイエンスコーパス: aminoguanidine

1 ic oxide synthase (NG-nitroarginine [NNA] or aminoguanidine).

2 pressed by prior treatment of the cells with aminoguanidine.

3 xemic mice co-administered the NOS inhibitor aminoguanidine.

4 the carbonyl-blocking reagents hydrazine and aminoguanidine.

5 OS2 knockout mice or in mice co-administered aminoguanidine.

6 fection, and the suppression was relieved by aminoguanidine.

7 and absence of incremental concentrations of aminoguanidine.

8 effect was prevented by coadministration of aminoguanidine.

9 ion that are prevented by the iNOS inhibitor aminoguanidine.

10 activity, which was completely prevented by aminoguanidine.

11 duced bacterial translocation was reduced by aminoguanidine.

12 tDNA from cultures treated with IL-1beta and aminoguanidine.

13 function, and this effect was ameliorated by aminoguanidine.

14 the inducible form of nitric oxide synthase, aminoguanidine.

15 NG-monomethyl-L-arginine, nitroarginine, and aminoguanidine.

16 T 486 are at least 20 times more potent than aminoguanidine.

17 adiated T98G cells, but it was diminished by aminoguanidine.

18 of the nitric oxide (NO) synthase inhibitor aminoguanidine.

19 re not suppressed by allopurinol but were by aminoguanidine.

20 tment of the animals with the iNOS inhibitor aminoguanidine.

21 on, and is blocked by the carbonyl scavenger aminoguanidine.

22 ted with the nitric oxide synthase inhibitor aminoguanidine.

23 antly increased in diabetes and inhibited by aminoguanidine.

24 activity of three phenylthiazole-substituted aminoguanidines.

25 (for MO-, GO-LDL) in the presence/absence of aminoguanidine (0, 1, 10, 100 microM).

26 ble nitric oxide, we examined the effects of aminoguanidine (0.5 mM).

27 tro-L-arginine-methyl ester (1.5 mmol/L) and aminoguanidine (1 mmol/L) block production of angiogenic

28 When NO production by iNOS was inhibited by aminoguanidine (1 mmol/L), there was a further increase

29 butylphenyl)-4-methylthiazol-5-yl)ethylidene)aminoguanidine (1) have been synthesized and tested agai

30 Aminoguanidine (100 mg/kg) was administered by intraperi

31 LDL (100 mg/l) for 3 days, with and without aminoguanidine (100 microM) in media.

32 Aminoguanidine (100 microM) present in culture media con

33 e inducible nitric oxide synthase inhibitor, aminoguanidine (30 mg/kg per dose), or a similar volume

34 after 7-nitroindazole (45 mumol/kg, s.c.) or aminoguanidine (30 mumol/kg, s.c.) administration was ev

35 synthase, whereas they were not affected by aminoguanidine (5 x 10(-5) mol/L), a specific inhibitor

36 the basis of its superior therapeutic ratio, aminoguanidine 69 was selected for preclinical developme

37 ve 29, aminopyridine 47, isothiourea 67, and aminoguanidine 69.

38 We also assessed the effects of aminoguanidine (a relatively selective iNOS inhibitor),

39 This reaction can be inhibited by aminoguanidine, a known inhibitor of AGE formation.

40 Aminoguanidine, a nonspecific inhibitor of iNOS, inhibit

41 Aminoguanidine, a nucleophilic hydrazine compound that p

42 Aminoguanidine, a pharmacological AGE inhibitor, was fou

43 nd acetaminophen-treated rats was blocked by aminoguanidine, a relatively specific inhibitor of iNOS.

44 treated a group of animals for 6 months with aminoguanidine, a relatively specific inhibitor of NOS-2

45 reatment of OBLV60-infected BALB/c mice with aminoguanidine, a selective inhibitor of iNOS activity,

46 Mice treated with aminoguanidine, a selective inhibitor of iNOS, exhibited

47 in mice with endothelial GR deficiency, and aminoguanidine, a specific iNOS inhibitor in mice was ab

48 NO synthesis was inhibited by treatment with aminoguanidine, a structural analogue of L-arginine.

49 If immunized rats were treated with aminoguanidine, a substrate inhibitor of NO synthase, at

50 We also examined the effects of aminoguanidine administered at 80 mg/kg i.p. immediately

51 Finally, an NOS-2 inhibitor, aminoguanidine, administered orally in the drinking wate

52 )-nitro-L-arginine-methyl ester (L-NAME), or aminoguanidine after delivery of PPD-coated beads to the

53 enzylacetamidine dihydrochloride (1400W) and aminoguanidine (AG) and a nonselective NOS antagonist, n

54 c oxide synthase (iNOS) selective inhibitors aminoguanidine (AG) and N6-(1-iminoethyl)-L-lysine (NIL)

55 aging we have evaluated the effectiveness of aminoguanidine (AG) as a neuroprotective agent in a rat

56 c inhibition of dietary AGE bioreactivity by aminoguanidine (AG) can improve turnover and renal excre

57 re-treatment of rats with the iNOS inhibitor aminoguanidine (AG) decreased the extent of NMDA-induced

58 in diabetes and aging, and the AGE inhibitor aminoguanidine (AG) has been shown to inhibit renal and

59 It is established that aminoguanidine (AG) is a metabolism-based inactivator of

60 Specific inhibition of NOS2 by aminoguanidine (AG) or L-NIL dramatically increased the

61 PS, and pretreatment with the iNOS inhibitor aminoguanidine (AG) partly restored the NE contraction.

62 del of IPS, continuous inhibition of NO with aminoguanidine (AG) reduced signs of IPS/GVHD, but also

63 of the nitric oxide (NO) synthesis inhibitor aminoguanidine (AG) to mice undergoing nonlethal graft-v

64 Aminoguanidine (AG) treatment, like nerve growth factor

65 of three selective type II NOS antagonists: aminoguanidine (AG), 2-amino-5,6-dihydro-6-methyl-4H-1,3

66 aims to investigate the modulatory effect of aminoguanidine (AG), an AGE inhibitor, in various stages

67 in focal cerebral ischemic damage exerted by aminoguanidine (AG), an inhibitor of inducible nitric ox

68 Treatment with an iNOS specific inhibitor, aminoguanidine (AG), of wild-type animals before infecti

69 f NO during GVHD, an NO synthesis inhibitor, aminoguanidine (AG), was administered to unirradiated (C

70 cts that are prevented by the iNOS inhibitor aminoguanidine (AG).

71 e antioxidants, N-acetyl-L-cysteine (NAC) or aminoguanidine (AG).

72 .) with saline or the NO synthase inhibitor, aminoguanidine (AG).

73 of the less potent, selective iNOS inhibitor aminoguanidine (AG); 500 ppm of the COX-2 inhibitor cele

74 p III, n=8]) or the selective iNOS inhibitor aminoguanidine (AG, 150 mg/kg SC [group V, n=7]) before

75 Group 3 (AG+A1, n = 6) was pretreated with aminoguanidine (AG, 50 mg/kg), and HCl was infused as ab

76 the animals were treated with 100 mg/kg i.v. aminoguanidine (AG, n=9); e) the fifth group received LP

77 Animals treated with iNOS inhibitor aminoguanidine (AG; 130 mg/kg every 8 h) had reduced NO

78 icrodialysis of a selective iNOS antagonist, aminoguanidine (AGN; 1.0 microM), for 60 min into the RV

79 ogation, and bioisosteric replacement of the aminoguanidine all were detrimental to antidiabetic acti

80 Inhibition of iNOS activity by aminoguanidine also attenuates TNF + LPS + IFN-gamma-ind

81 Aminoguanidine also increased twitch Ca(2+) transient am

82 Fluorospectrometry examination showed that aminoguanidine also inhibited the formation of fluoresce

83 Aminoguanidine also significantly improved the histologi

84 ls, but not allograft parenchymal cells; (2) aminoguanidine ameliorated the histological and function

85 infected with BCG-TNF, inhibition of iNOS by aminoguanidine (AMG) abolished the killing of the bacill

86 ontrols (n = 8), untreated diabetic (n = 8), aminoguanidine (AMG)-treated diabetic (2.5 g/kg of diet;

87 Some rats were pretreated with aminoguanidine (AMG, 50 mg/Kg BW in drinking water) befo

88 eliminated by treating the cells with either aminoguanidine (an inhibitor of inducible nitric oxide (

89 Previous studies have shown that aminoguanidine, an AGE inhibitor, can prevent glucose cr

90 More importantly, a pronounced effect of aminoguanidine, an AGE-formation inhibitor, was observed

91 e (iNOS), and the induction was inhibited by aminoguanidine, an inhibitor of iNOS.

92 Aminoguanidine, an iNOS inhibitor, also attenuated infar

93 The corresponding aminoguanidine analogue 2 was recently discovered to ret

94 nduced cell death, whereas the NO inhibitors aminoguanidine and 2-(4-carboxyphenyl)-4,4,5,5-tetra-met

95 In contrast, the respective Cl(in) of [14C]aminoguanidine and [14C]guanidine (0.0085+/-0.00039 and

96 guanidino substrates, [14C]L-arginine, [14C]aminoguanidine and [14C]guanidine, in the presence or ab

97 n in LPS-treated skin was also suppressed by aminoguanidine and allopurinol independently.

98 al hyperpermeability was ameliorated by both aminoguanidine and another selective iNOS inhibitor, S-m

99 Effects of aminoguanidine and aspirin on the development of retinop

100 ly distinct inhibitors of polyamine oxidase (aminoguanidine and chloroquine) attenuates brain polyami

101 is to histologically evaluate the effects of aminoguanidine and doxycycline in the modification of pe

102 ceptor 2 and Akt/PKB as well as MG scavenger aminoguanidine and glo1 activation prevented MG-induced

103 ggest that the hydrophilic guanidino cations aminoguanidine and guanidine penetrate the BBB by a mino

104 as 1000x concentrations of nitro-L-arginine, aminoguanidine and guanidine were without effect.

105 Aminoguanidine and iodonium diphenyl, mechanistically un

106 with vehicle or with 1 of 2 iNOS inhibitors (aminoguanidine and L-N-iminoethyl-lysine), administered

107 Aminoguanidine and mercaptoethylguanidine (MEG) are inhi

108 We examined the effects of aminoguanidine and methylguanidine on vascular dysfuncti

109 d by nitric oxide synthase (NOS) inhibitors (aminoguanidine and N(G)-monomethyl L-arginine).

110 e NONOate, whereas the NO synthase inhibitor aminoguanidine and NO scavenger 2-(4-carboxyphenyl)-4,4,

111 AGE inhibitors such as aminoguanidine and pyridoxamine (PM) have proven effecti

112 AGE inhibitors such as aminoguanidine and pyridoxamine (PM) inhibit both the fo

113 or copper ranged from approximately 2 mm for aminoguanidine and pyridoxamine, to 10-100 microm for ca

114 s of advanced glycation end products (AGEs), aminoguanidine and pyridoxamine, to inhibit and regress

115 Two known inhibitors of AGE formation, aminoguanidine and rifampicin, were applied during CXL i

116 In contrast aminoguanidine and S-methylisothiourea sulphate (two ind

117 ndazole, N(G)-nitro-L-arginine methyl ester, aminoguanidine and S-methylisothiourea sulphate) in this

118 was inhibited by the iNOS-specific inhibitor aminoguanidine and the tyrosine kinase inhibitor geniste

119 ewis rats, and diabetic animals treated with aminoguanidine and two novel advanced glycosylation end

120 in vivo screens designed to test efficacy of aminoguanidine and two novel AGE-formation inhibitors, A

121 nhibition by established inhibitors, such as aminoguanidine, and for searching for novel inhibitors s

122 Inhibitors of nitric oxide synthase, aminoguanidine, and N(G)-monomethyl-L-arginine, attenuat

123 cross-link K2P was decreased by NC-I, NC-II, aminoguanidine, and pyridoxamine (P = NS).

124 We treated DBA/2 mice with aminoguanidine, and they became more susceptible to C. i

125 ormalization of solubility was observed with aminoguanidine at 100 mg/kg body wt, whereas a similar n

126 mma, depleted of neutrophils or treated with aminoguanidine at the time of reinfection, maintained an

127 ed glycation end product formation inhibitor aminoguanidine attenuated HG-induced Ang II generation.

128 he NOS inhibitors N(G)-methyl-L-arginine and aminoguanidine both inhibited nitrite production and pre

129 Aminoguanidine (but not aspirin) inhibited a diabetes-in

130 Administration of aminoguanidine continuously from the time of induction o

131 We gave group 4 animals aminoguanidine daily for 6 months, which prevented abnor

132 Aminoguanidine did not affect ischemic brain swelling (p

133 Aminoguanidine did not affect the mild histological chan

134 treatment of Tg mice with the iNOS inhibitor aminoguanidine did not alter the level of protection aff

135 or inhibition of inducible NO synthesis with aminoguanidine did not change bile flow, although pretre

136 Rats that received aminoguanidine did not show this increase in protein and

137 tion of hepcidin transcription by cytokines: aminoguanidine does not inhibit the stimulation of hepci

138 -1-oxyl-3-oxide and by NO synthase inhibitor aminoguanidine effectively inhibited S-nitrosylation of

139 tion activity ranged between 250 and 711mmol aminoguanidine Eq/kg.

140 Administration of aminoguanidine essentially prevented the retinopathy, si

141 -yielding method for the preparation of N(G)-aminoguanidines from primary amines is reported.

142 neutralizing TNF mAb and the iNOS inhibitor, aminoguanidine, further suggesting that TNF and iNOS are

143 At aminoguanidine-glucose molar ratios of 1:8 to 1:1, 26 to

144 At aminoguanidine-glucose molar ratios of 1:8 to 1:1, fluor

145 TAC and MMF; group 3, low-dose TAC, MMF, and aminoguanidine; group 4, low-dose TAC, MMF, and arginine

146 for analogs containing S-alkylisothiourea or aminoguanidine groups.

147 cible nitric oxide synthase (iNOS) inhibitor aminoguanidine had no effect on baselines or increases i

148 lterations in acetaminophen metabolism since aminoguanidine had no effect on hepatocyte cytochrome P4

149 ine in tail collagen and aorta, and Hb-AGE), aminoguanidine had no significant influence on these par

150 The biochemical mechanism by which aminoguanidine has inhibited retinopathy thus is not cle

151 munosuppression by in vivo administration of aminoguanidine hemisulfate (AG).

152 cible nitric oxide synthase (iNOS) inhibitor aminoguanidine hydrochloride, arginase inhibitor N-hydro

153 mpicin inhibited CXL more significantly than aminoguanidine in gel electrophoresis and tensile streng

154 imary amines are converted to protected N(G)-aminoguanidines in a one-pot procedure.

155 tion that is caused, at least in part, by an aminoguanidine-inhibitable mechanism.

156 anti-AGE-keyhole limpet hemocyanin antibody, aminoguanidine inhibited glucose-induced N(epsilon)-(car

157 Aminoguanidine inhibited lipopolysaccharide-induced incr

158 change bile flow, although pretreatment with aminoguanidine inhibited NO production by 85%.

159 Treatment with the selective iNOS inhibitor, aminoguanidine, inhibited iNOS enzymatic activity and ov

160 Macrophage depletion, aminoguanidine inhibition of iNOS, and neutralization of

161 Glycation-linked aminoguanidine-insensitive processes, however, such as t

162 e inducible nitric oxide synthase inhibitor (aminoguanidine) into the renal artery for 2 hrs after th

163 If aminoguanidine is similarly active in vivo, this compoun

164 otential that may complement others, such as aminoguanidine, known to either prevent initial sugar at

165 significantly ameliorated by the addition of aminoguanidine, L-N(G)-monomethyl arginine, or Tiron.

166 s to determine whether low concentrations of aminoguanidine might prevent cytotoxic modification of L

167 Very low concentrations of aminoguanidine mitigate toxicity of LDL exposed to stres

168 Radical adduct formation was suppressed by aminoguanidine, N-(3-aminomethyl)benzylacetamidine (1400

169 Aminoguanidine neither affected the oxidation of cytochr

170 o-L-arginine methyl ester and a high dose of aminoguanidine normalized renal blood flow, but did not

171 may contribute to the beneficial effects of aminoguanidine observed in experimental diabetic retinop

172 These discordant effects of aminoguanidine on diabetes-induced vascular changes vers

173 There was no effect of aminoguanidine on forskolin-stimulated CaSpF in normal m

174 s of inducible nitric oxide synthase (iNOS) (aminoguanidine or 1400W).

175 creased by 1000x concentrations of unlabeled aminoguanidine or guanidine.

176 ors of nitric-oxide synthase (NOS) activity, aminoguanidine or N-monomethyl-L-arginine, was evaluated

177 pretreatments: a) selective iNOS inhibitors aminoguanidine or S-methylisothiourea; b) 3-morpholinosy

178 stration of nitric oxide synthase inhibitor (aminoguanidine) or by CD4(+) T-cell depletion.

179 if LDL had been modified in the presence of aminoguanidine (P < 0.001).

180 prevented with the selective iNOS inhibitor aminoguanidine (PaO2 of 566+/-19, 76+/-22, and 504+/-105

181 sence or presence of the glycation inhibitor aminoguanidine (pimagedine).

182 received LPS and 1 hr later was treated with aminoguanidine plus inhaled NO (AG+NO, n=7).

183 Aminoguanidine present during LDL modification had no ef

184 iNOS inhibition with aminoguanidine prevented or attenuated allograft heart a

185 Treatment with the selective iNOS inhibitor aminoguanidine prevented T/HS lymph-induced lung injury.

186 parental mice with a NO synthase inhibitor, aminoguanidine, prevented early death in these mice as w

187 We demonstrate that although aminoguanidine, pyridoxamine, and BMP-7 significantly in

188 oup) were fed a diet containing 0.1% (wt/wt) aminoguanidine, pyridoxamine, penicillamine, and nucleop

189 Aminoguanidine reduced albuminuria by 70% after 4 months

190 formin and the structurally related compound aminoguanidine reduced DNA damage and ameliorated sponta

191 The iNOS inhibitor aminoguanidine reduced PGE2 concentration in the infarct

192 n inducible nitric oxide synthase inhibitor, aminoguanidine, reduced DOX-induced mortality and improv

193 nine-binding sites occupied by imidazole and aminoguanidine, respectively, provide a template for des

194 ction by the nitric oxide synthase inhibitor aminoguanidine resulted in reactivation.

195 d livers from immunized animals treated with aminoguanidine revealed fewer and smaller cellular infil

196 Neither NNA nor aminoguanidine reversed the depression in atrial functio

197 Because aminoguanidine's neuroprotective properties have primari

198 mental conditions) do not support a role for aminoguanidine-sensitive processes in the development of

199 Aminoguanidine shows little inhibition of post-Amadori A

200 Administration of aminoguanidine significantly inhibited the I/R-induced c

201 activation of beta-catenin was attenuated by aminoguanidine, suggesting that oxidative stress is a di

202 Furthermore, aminoguanidine suppressed the AGE formation on beta2M bo

203 es on osseointegration can be modified using aminoguanidine systemically.

204 Chronic aminoguanidine therapy did not diminish the frequency or

205 (-/-) NOS2(-/-) and gp91phox(-/-) mice given aminoguanidine [to suppress the effects of nitric oxide

206 504+/-105 mmHg for isograft, allograft, and aminoguanidine-treated allograft, respectively; P<0.0002

207 Eyes of aminoguanidine-treated animals with similar elevations o

208 of mucosal oxygen consumption was higher in aminoguanidine-treated as compared with vehicle-treated

209 Aminoguanidine-treated diabetic animals had a significan

210 the eyes with similarly elevated IOP in the aminoguanidine-treated group lost less than 10% of their

211 ers of dispersed lung cells from L-NAME- and aminoguanidine-treated mice produced significantly highe

212 AB was more severe than that of DeltarpfB in aminoguanidine-treated mice.

213 Furthermore, aminoguanidine treatment did not affect the development

214 and GFAP protein expression were blocked by aminoguanidine treatment in the hypertensive retina.

215 nce of NO is illustrated by the finding that aminoguanidine treatment leads to more severe liver dise

216 In vivo nicotinamide or aminoguanidine treatment of prediabetic ZDF rats prevent

217 In the present studies, the effects of aminoguanidine treatment on ultrastructural changes in t

218 Aminoguanidine treatment significantly increased RGC sur

219 Aminoguanidine treatment significantly reduced expressio

220 ctivation of latent tuberculous infection by aminoguanidine treatment was confirmed using a second mu

221 One group of diabetic rats was given aminoguanidine via intraperitoneal injection, and anothe

222 Aminoguanidine was administered at 80 mg/kg i.p. immedia

223 Aminoguanidine was as effective at 1 microM as at the hi

224 Pretreatment of rats with aminoguanidine was found to prevent acetaminophen-induce

225 By extracellular trapping with aminoguanidine, we established that these oxo-aldehydes

226 In the infected mice treated for 2 wk with aminoguanidine, we observed an increase in the number of

227 dies revealed that the inhibitory effects of aminoguanidine were due predominantly to inhibition of i

228 Glucose and aminoguanidine were then removed by dialysis.

229 el mono- and symmetrical di-N-hydroxy- and N-aminoguanidines were readily prepared from the reaction

230 Aminoguanidine, which has been found to inhibit the deve

231 n media transfer protocols, while c-PTIO and aminoguanidine, which lower nitric oxide levels, prevent

232 educed insulin output; both nicotinamide and aminoguanidine, which lower NO, prevented the FFA-mediat

233 Aminoguanidine, which prevents formation of advanced gly

234 described for a variety of N-hydroxy- and N-aminoguanidines with different substitution patterns in

235 man melanocytes and as this was inhibited by aminoguanidine would appear to involve an induction of i