Assessment of Sodium Butyrate’s Pharmacological Effects on Gentamicin-induced Nephrotic Disorders in a Rat Model

Background Sodium butyrate (SB) used to increase oxidative stress was reduced and the glutathione redox pathway was boosted. It inhibits proliferation, induction of differentiation, and induction or repression of gene expression and it has also anti-inflammatory action. This is endorsed for suppression of nephrotic symptoms. Objectives The present study was carried out to evaluate the nephroprotective activity of SB on gentamicin-induced nephrotoxicity in rats. Materials and Methods Present research work was designed to estimate pharmacological potential of SB in gentamicin-induced nephrotic disorder. The pharmacological prospective was estimated in gentamicin-induced rats through the oral administration of SB formulation 200 mg/kg and 300 mg/kg BW. Results The study observed that the SB significantly protects the kidneys from gentamicin-induced nephrotic disorders. Gentamicin 100 mg/kg for 7 days was used for induction of nephrotoxicity in Wistar rats by intraperitoneal administration. The administration of SB was observed to decrease the occurrence of glomerular congestion, vascular congestion, epithelial desquamation, inflammatory cell build-up, and kidney cell necrosis induced by gentamicin. The dose of SB maintained the gentamicin-induced increased creatinine (0.62±0.05), serum urea (18.10±0.79), uric acid (2.10±0.28), and blood urea nitrogen (BUN) (17.56±0.55) levels. This fact is further sustained by the histopathological examinations. Conclusion Sodium butyrate formulation with antinephrotic activity in maintaining uremic solutes such as urea, uric acid, creatinine, BUN, ketone, urobilinogen, glucose, specific gravity, and urine pH in Wistar rats with gentamicin-induced glomerulonephritis (GN). The SB was administered to the animals at doses of 200 and 300 mg/kg body weight. Pretreatment with the drug showed promising results in maintaining elevated parameters in nephritic rats within a short duration.

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Journal
Journal of Pharmacology and Pharmacotherapeutics
Published
2024-09-16
DOI
https://doi.org/10.1177/0976500x241271468
Citations
1
Primary Topic
Antibiotics Pharmacokinetics and Efficacy
Type
article
Field-Weighted Citation Impact
0.45
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article

Assessment of Sodium Butyrate’s Pharmacological Effects on Gentamicin-induced Nephrotic Disorders in a Rat Model

Rakesh K. Sindhu, Sunil Kumar
1 citations
Journal of Pharmacology and Pharmacotherapeutics
Antibiotics Pharmacokinetics and Efficacy
0.45
article

Assessment of Sodium Butyrate’s Pharmacological Effects on Gentamicin-induced Nephrotic Disorders in a Rat Model

Rakesh K. Sindhu, Sunil Kumar
article en
1 citations

Abstract

Background Sodium butyrate (SB) used to increase oxidative stress was reduced and the glutathione redox pathway was boosted. It inhibits proliferation, induction of differentiation, and induction or repression of gene expression and it has also anti-inflammatory action. This is endorsed for suppression of nephrotic symptoms. Objectives The present study was carried out to evaluate the nephroprotective activity of SB on gentamicin-induced nephrotoxicity in rats. Materials and Methods Present research work was designed to estimate pharmacological potential of SB in gentamicin-induced nephrotic disorder. The pharmacological prospective was estimated in gentamicin-induced rats through the oral administration of SB formulation 200 mg/kg and 300 mg/kg BW. Results The study observed that the SB significantly protects the kidneys from gentamicin-induced nephrotic disorders. Gentamicin 100 mg/kg for 7 days was used for induction of nephrotoxicity in Wistar rats by intraperitoneal administration. The administration of SB was observed to decrease the occurrence of glomerular congestion, vascular congestion, epithelial desquamation, inflammatory cell build-up, and kidney cell necrosis induced by gentamicin. The dose of SB maintained the gentamicin-induced increased creatinine (0.62±0.05), serum urea (18.10±0.79), uric acid (2.10±0.28), and blood urea nitrogen (BUN) (17.56±0.55) levels. This fact is further sustained by the histopathological examinations. Conclusion Sodium butyrate formulation with antinephrotic activity in maintaining uremic solutes such as urea, uric acid, creatinine, BUN, ketone, urobilinogen, glucose, specific gravity, and urine pH in Wistar rats with gentamicin-induced glomerulonephritis (GN). The SB was administered to the animals at doses of 200 and 300 mg/kg body weight. Pretreatment with the drug showed promising results in maintaining elevated parameters in nephritic rats within a short duration.

Journal of Pharmacology and PharmacotherapeuticsVol. 15(4)
Sharda University (IN)
Openalex Percentile: Top 31%
Antibiotics Pharmacokinetics and Efficacy
0.45
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