ライフサイエンスコーパス: aminoguanidine

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

2 xemic mice co-administered the NOS inhibitor aminoguanidine.

3 the carbonyl-blocking reagents hydrazine and aminoguanidine.

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

5 fection, and the suppression was relieved by aminoguanidine.

6 pressed by prior treatment of the cells with 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 ted in the presence of the aldehyde quencher aminoguanidine.

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

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

20 re not suppressed by allopurinol but were by aminoguanidine.

21 tment of the animals with the iNOS inhibitor aminoguanidine.

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

23 ted with the nitric oxide synthase inhibitor aminoguanidine.

24 antly increased in diabetes and inhibited by aminoguanidine.

25 activity of three phenylthiazole-substituted aminoguanidines.

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

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

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

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

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

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

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

33 Aminoguanidine (100 microM) present in culture media con

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

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

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

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

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

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

40 Aminoguanidine, a deglycation agent, rescued the comprom

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

42 Aminoguanidine, a nonspecific inhibitor of iNOS, inhibit

43 Aminoguanidine, a nucleophilic hydrazine compound that p

44 Aminoguanidine, a pharmacological AGE inhibitor, was fou

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

66 Aminoguanidine (AG) treatment, like nerve growth factor

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

85 Aminoguanidine also significantly improved the histologi

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

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

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

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

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

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

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

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

94 Aminoguanidine, an iNOS inhibitor, also attenuated infar

95 The corresponding aminoguanidine analogue 2 was recently discovered to ret

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

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

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

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

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

101 Effects of aminoguanidine and aspirin on the development of retinop

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

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

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

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

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

107 Aminoguanidine and iodonium diphenyl, mechanistically un

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

109 Aminoguanidine and mercaptoethylguanidine (MEG) are inhi

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

132 The aminoguanidine compound robenidine is widely used as an

133 ded toward the synthesis of novel anticancer aminoguanidine compounds.

134 Administration of aminoguanidine continuously from the time of induction o

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

136 Aminoguanidine did not affect ischemic brain swelling (p

137 Aminoguanidine did not affect the mild histological chan

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

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

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

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

142 -1-oxyl-3-oxide and by NO synthase inhibitor aminoguanidine effectively inhibited S-nitrosylation of

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

144 Administration of aminoguanidine essentially prevented the retinopathy, si

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

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

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

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

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

150 for analogs containing S-alkylisothiourea or aminoguanidine groups.

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

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

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

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

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

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

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

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

159 tors, N(G)-nitro-L-arginine methyl ester and aminoguanidine; in addition, the expression of NOS isofo

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

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

162 Aminoguanidine inhibited lipopolysaccharide-induced incr

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

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

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

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

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

168 If aminoguanidine is similarly active in vivo, this compoun

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

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

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

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

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

174 Aminoguanidine neither affected the oxidation of cytochr

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

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

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

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

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

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

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

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

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

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

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

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

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

188 Aminoguanidine present during LDL modification had no ef

189 iNOS inhibition with aminoguanidine prevented or attenuated allograft heart a

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

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

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

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

194 Aminoguanidine reduced albuminuria by 70% after 4 months

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

196 The iNOS inhibitor aminoguanidine reduced PGE2 concentration in the infarct

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

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

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

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

201 Neither NNA nor aminoguanidine reversed the depression in atrial functio

202 Because aminoguanidine's neuroprotective properties have primari

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

204 Aminoguanidine shows little inhibition of post-Amadori A

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

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

207 Furthermore, aminoguanidine suppressed the AGE formation on beta2M bo

208 es on osseointegration can be modified using aminoguanidine systemically.

209 Chronic aminoguanidine therapy did not diminish the frequency or

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

211 504+/-105 mmHg for isograft, allograft, and aminoguanidine-treated allograft, respectively; P<0.0002

212 Eyes of aminoguanidine-treated animals with similar elevations o

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

214 Aminoguanidine-treated diabetic animals had a significan

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

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

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

218 Furthermore, aminoguanidine treatment did not affect the development

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

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

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

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

223 Aminoguanidine treatment significantly increased RGC sur

224 Aminoguanidine treatment significantly reduced expressio

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

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

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

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

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

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

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

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

233 Glucose and aminoguanidine were then removed by dialysis.

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

235 Aminoguanidine, which has been found to inhibit the deve

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

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

238 Aminoguanidine, which prevents formation of advanced gly

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

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