Improving effect of aminoguanidine on lipopolysaccharide-caused kidney dysfunction in rats

Abstract EN

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.