Protective Effects of Valsartan on Gentamicin Induced Tubular Injury through Down Regulation of Urinary N-Acetyl-Β-D-Glucosaminidase in Rats.

Urinary N-acetyl-β-D-glucosaminidase is a marker of early tubular damage. Therefore, the current study was to investigate effects and its underling mechanisms of valsartan on gentamicin induced renal tubular injury through urinary N-acetyl-β-D-glucosaminidase parameter variety in rats. Animals were divided into four groups consisting of 12 rats each. The study lasted for 10 d. Rats were treated in two batches on the 6th and 11th d of the experiment, with 6 rats in each group. Control group rats were administered with distilled water (10 ml/kg) daily via an intragastric gavage; gentamicin group rats were given gentamicin 100 mg/kg/d intraperitoneally; valsartan (10 mg/kg/d, intragastric gavage) +gentamicin group; valsartan (20 mg/kg/d, intragastric gavage) +gentamicin group. Rats treated with gentamicin showed significant elevation in the activity and expression of urinary N-acetyl-β-D-glucosaminidase as compared with the control group; the activities of superoxide dismutase, glutathione peroxidase and catalase were lower while malondialdehyde was higher in kidney tissues; urinary protein content was not changed; serum creatinine and blood urea nitrogen were increased. Moreover, pathological damage of the renal tubules was serious in gentamicin treated rats. Valsartan significantly inhibited activity and expression of urinary N-acetyl-β-D-glucosaminidase in a dose dependent manner; dramatically increased superoxide dismutase, glutathione peroxidase and catalase activities and markedly decreased malondialdehyde levels in kidney tissues; renal tubular structural damages were also effectively ameliorated by valsartan. These results show that changes of urinary N-acetyl-β-Dglucosaminidase levels can reflect the extent of renal tubular injury, that valsartan has protective role on gentamicin-induced renal tubular injury by down-regulation urinary N-acetyl-β-D-glucosaminidase, and its down-regulation urinary N-acetyl-β-D-glucosaminidase effect may be due to its antioxidant properties in kidney tissues. [ABSTRACT FROM AUTHOR]