Aminoguanidine hydrochloride is a diamine oxidase and NO synthase inhibitor, reduces levels of advanced glycation end products (AGEs) through interacting with 3-deoxyglucosone, is an investigational drug for the treatment of diabetic nephropathy. Combination of sub-threshold dose of meloxicam (1 mg/kg) with increasing doses of aminoguanidine hydrochloride (30, 100 and 300 mg/kg) resulted in synergistic anti-inflammatory effect. Combined therapy with sub-threshold dose of aminoguanidine hydrochloride (30 mg/kg) with increasing doses of meloxicam (1, 3, 10 and 30 mg/kg) also resulted in synergistic anti-inflammatory effect[3]. Combination of a subthreshold dose of rofecoxib (1 mg/kg) with increasing doses of aminoguanidine hydrochloride (30, 100 and 300 mg/kg) resulted in potentiated antinociception. Combined therapy with a subthreshold dose of aminoguanidine hydrochloride (30 mg/kg) with increasing doses of rofecoxib (1, 3, 10 and 30 mg/kg) also resulted in significant antinociception. Thus, rofecoxib and aminoguanidine hydrochloride act synergistically in their antinociceptive action in mice[4]. The fever index calculated for rats pretreated with v-LNIO or with aminoguanidine and injected with LPS (lipopolisaccharide) was reduced by 43% and 72%, respectively, compared to that calculated for water-pretreated and LPS-injected rats. Whereas vL-NIO (Vinyl-L-NIO (N(5) - (1-Imino-3-butenyl) - ornithine) partly attenuated both phases of febrile rise in T(b), administration of aminoguanidine into the brain completely prevented fever induced by LPS[5].
Aminoguanidine HCl/氨基胍盐酸盐 细胞实验
Cell Line
Concentration
Treated Time
Description
References
MDA-MB-468 cells
1 mM
24-48 hours
To study the effect of NOS2 inhibition on cell migration and biomarker expression, results showed AG suppressed NOS2 expression and activity.
Proc Natl Acad Sci U S A. 2014 Apr 29;111(17):6323-8.
MDA-MB-231 cells
1 mM
24-48 hours
To study the effect of NOS2 inhibition on cell migration and biomarker expression, results showed AG suppressed NOS2 expression and activity.
Proc Natl Acad Sci U S A. 2014 Apr 29;111(17):6323-8.
MCF-7 cells
1 mM
24-48 hours
To study the effect of NOS2 inhibition on cell migration and biomarker expression, results showed AG suppressed NOS2 expression and activity.
Proc Natl Acad Sci U S A. 2014 Apr 29;111(17):6323-8.
Mouse C8-B4 microglial cells
10 μM
24 hours
Aminoguanidine, an iNOS inhibitor, abolished the lipopolysaccharide and IFNγ-induced decrease in cell viability.
Anesthesiology. 2009 Sep;111(3):566-73.
Aminoguanidine HCl/氨基胍盐酸盐 动物实验
Species
Animal Model
Administration
Dosage
Frequency
Description
References
Nude mice
MDA-MB-231-GFP breast cancer xenograft model
Oral administration in drinking water
0.5 g/L
Continuous administration for 37 days
To study the effect of NOS2 inhibition on tumor growth and metastasis, results showed AG significantly reduced tumor growth and metastasis.
Proc Natl Acad Sci U S A. 2014 Apr 29;111(17):6323-8.
Tg2576 mice
Alzheimer's disease model
Subcutaneous injection
20 mg/ml
Once daily for 3 months
To investigate the inhibitory effect of aminoguanidine on glycated Aβ formation and its impact on cognitive function, results showed that aminoguanidine significantly reduced levels of AGEs and Aβ, and improved spatial learning and memory in mice.
Cell Death Dis. 2013 Jun 13;4(6):e673
Mice
Endothelial-specific GR knockout mice (GREC KO)
Intraperitoneal injection
15 mg/kg
Administered at +2, +6, +24, and +30 hours after LPS treatment
To evaluate the protective effect of aminoguanidine against LPS-induced sepsis. Results showed that aminoguanidine significantly improved the survival rate of GREC KO mice, nearly to 100%.
Proc Natl Acad Sci U S A. 2013 Jan 2;110(1):306-11.
C57BL/6J mice
STZ-induced diabetic model
Tail vein injection
100 mg/kg/day
Once daily for three days
Aminoguanidine significantly attenuated aortic hydrogen peroxide (H2O2) production in diabetic aortas but had only a marginal effect on reducing aortic superoxide (O2?-) production. The endothelium-dependent vasodilatation was modestly but significantly improved by AG, likely due to AG-induced reduction in hypercontractility. In endothelium-denuded diabetic aortas, NAD(P)H oxidase (NOX)-dependent O2?- production was completely attenuated by AG.
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