Aminoguanidine affects systemic and lung inflammation induced by lipopolysaccharide in rats

BackgroundNitric oxide is a mediator of potential importance in numerous physiological and inflammatory processes in the lung. Aminoguanidine (AG) has been shown to have anti-inflammation and radical scavenging properties. This study aimed to investigate the effects of AG, an iNOS inhibitor, on lipopolysaccharide (LPS)-induced systemic and lung inflammation in rats.MethodsMale Wistar rats were divided into control, LPS (1mg/kg/day i.p.), and LPS groups treated with AG 50, 100 or 150mg/kg/dayi.p. for five weeks. Total nitrite concentration, total and differential white blood cells (WBC) count, oxidative stress markers, and the levels of IL-4, IFN-, TGF-1, and PGE2 were assessed in the serum or bronchoalveolar lavage fluid (BALF).ResultsAdministration of LPS decreased IL-4 level (p<0.01) in BALF, total thiol content, superoxide dismutase (SOD) and catalase (CAT) activities (p<0.001) in BALF and serum, and increased total nitrite, malondialdehyde (MDA), IFN-, TGF-1 and PGE2 (p<0.001) concentrations in BALF. Pre-treatment with AG increased BALF level of IL-4 and total thiol as well as SOD and CAT activities (p<0.05 to p<0.001), but decreased BALF levels of total nitrite, MDA, IFN-, TGF-1, and PGE2 (p<0.01 to p<0.001). AG treatment decreased total WBC count, lymphocytes and macrophages in BALF (p<0.01 to p<0.001) and improved lung pathological changes including interstitial inflammation and lymphoid infiltration (p<0.05 to p<0.001).ConclusionsAG treatment reduced oxidant markers, inflammatory cytokines and lung pathological changes but increased antioxidants and anti-inflammatory cytokines. Therefore, AG may play a significant protective role against inflammation and oxidative stress that cause lung injury.