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Saudi Journal of Kidney Diseases and Transplantation
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ORIGINAL ARTICLE Table of Contents   
Year : 2020  |  Volume : 31  |  Issue : 5  |  Page : 1025-1033
Improving Effect of Aminoguanidine on Lipopolysaccharide-Caused Kidney Dysfunction in Rats

1 Neurogenic Inflammation Research Center, Mashhad University of Medical Sciences, Mashhad, Iran
2 Neuroscience Research Center; Department of Physiology, School of Paramedical Sciences, Torbat Heydariyeh University of Medical Sciences, Torbat Heydariyeh, Iran
3 Department of Physiology, School of Medicine, Jiroft University of Medical Sciences, Jiroft, Iran

Correspondence Address:
Akbar Anaeigoudari
Department of Physiology, School of Medicine, Jiroft University of Medical Sciences, Jiroft
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/1319-2442.301167

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Kidneys have been shown to be the main target for toxins. Lipopolysaccharide (LPS) is a bacterial endotoxin which can involve in pathogenesis of endotoxemia-caused kidney dysfunction. Excessive production of free radicals such as nitric oxide (NO) and pro-inflammatory cytokines have been reported to contribute in kidney dysfunction. The purpose of this study was to investigate the effect of inducible nitric oxide synthase (iNOS) inhibition against LPS-induced kidney dysfunction in rats. Male rats were assigned into five groups. Control animals were injected saline; LPS group received 1 mg/kg of LPS for five weeks; LPS-AG50, LPS-AG100, and LPS-AG150 groups received AG (50, 100, and 150 mg/kg, respectively) 30 min before LPS. All drugs were administered intraperitoneally. LPS injection enhanced the level of blood urea nitrogen (BUN) and creatinine compared with the control group. Pretreatment with AG resulted in a significant reduction in BUN and creatinine in LPS-AG100 and LPS-AG 150 groups with respect to the LPS group. LPS administration led to a significant increase in interleukin (IL)-6, malondialdehyde (MDA), and NO metabolites as well as a significant decrease in the content of total thiol groups and superoxide dismutase (SOD) and catalase (CAT) activity. Pretreatment with AG reduced the level of IL-6, MDA, and NO metabolites and enhanced the content of total thiol groups and SOD and CAT activity in LPS-AG groups compared to the LPS group. The results of the present study show that inhibition of iNOS has a protective effect against kidney dysfunction caused by LPS.

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