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].
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