Protective effects of valsartan on gentamicin induced tubular injury through down regulation of urinary N-acetyl-Y-D-glucosaminidase in rats
By: Li, Qi Xiong
.
Contributor(s): Jiang, Xiao Ye.
Publisher: Mumbai Indian Journal of Pharmaceutical Science 2021Edition: Vol.83(1), Jan-Feb.Description: 69-75p.Subject(s): PHARMACEUTICSOnline resources: Click here
In:
Indian journal of pharmaceutical sciencesSummary: 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 6 th and 11 th 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-D-
glucosaminidase levels can re flect 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.
| Item type | Current location | Call number | Status | Date due | Barcode | Item holds |
|---|---|---|---|---|---|---|
Articles Abstract Database
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School of Pharmacy Archieval Section | Not for loan | 2021-2022626 |
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 6 th and 11 th 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-D-
glucosaminidase levels can re flect 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.
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