Please use this identifier to cite or link to this item: https://doi.org/10.1016/S0014-2999(96)00677-2
Title: Expression of inducible nitric oxide synthase in mice: Pharmacological evaluation of adenosine receptor agonists
Authors: Moochhala, S.M. 
Hon, W.-M.
Chhatwal, V.J.S.
Khoo, H.-E. 
Keywords: Adenosine
Anti-inflammatory
mRNA expression
Nitric oxide (NO)
Nitric oxide (NO) synthase
Issue Date: 5-Dec-1996
Source: Moochhala, S.M., Hon, W.-M., Chhatwal, V.J.S., Khoo, H.-E. (1996-12-05). Expression of inducible nitric oxide synthase in mice: Pharmacological evaluation of adenosine receptor agonists. European Journal of Pharmacology 316 (2-3) : 287-296. ScholarBank@NUS Repository. https://doi.org/10.1016/S0014-2999(96)00677-2
Abstract: Inhibition of inducible nitric oxide (NO) synthase during endotoxaemia may be of therapeutic value. We have previously shown that pretreatment of mice with adenosine receptor agonists 1 h before lipopolysaccharide administration results in a dose-dependent reduction of plasma nitrite and nitrate (NO(x)-)) levels. This report examines the effects of adenosine receptor agonists, 5'-N-ethylarboxamidoadenosine (NECA), N6-cyclohexyladenosine (CHA), R-phenylisopropyl-adenosine (R-PIA) and 5'-(N-cyclopropyl)carboxamidoadenosine (CPCA), on the level of inducible NO synthase expression in a model of liver inflammation induced by lipopolysaccharide. Following lipopolysaccharide administration (10 mg/kg, i.p.), liver mRNA expression peaked at 3 h and declined to 35% of maximal level after 24 h. Pretreatment with adenosine receptor agonists (0.001 mg/kg to 5 mg/kg, i.p.) depressed inducible NO synthase mRNA expression significantly. Down-regulation of inducible NO synthase mRNA expression corresponded with changes in plasma NO(x)- level as well as activity of NO synthase in the liver. Administration of R-PIA (5 mg/kg, i.p.) increased the survival of animals injected with a lethal dose of lipopolysaccharide. Thus adenosine receptor agonists may useful as anti-inflammatory agents in the treatment of endotoxaemia.
Source Title: European Journal of Pharmacology
URI: http://scholarbank.nus.edu.sg/handle/10635/107788
ISSN: 00142999
DOI: 10.1016/S0014-2999(96)00677-2
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