The nephroprotective potential of selected synthetic compound against gentamicin induced nephrotoxicity.


Journal

BMC pharmacology & toxicology
ISSN: 2050-6511
Titre abrégé: BMC Pharmacol Toxicol
Pays: England
ID NLM: 101590449

Informations de publication

Date de publication:
27 Sep 2024
Historique:
received: 30 04 2024
accepted: 15 07 2024
medline: 28 9 2024
pubmed: 28 9 2024
entrez: 28 9 2024
Statut: epublish

Résumé

Nephrotoxicity, the rapid impairment of kidney function caused by harmful drugs and chemicals, affects about 20% of cases and is projected to become a leading cause of death by reactive oxygen species (ROS). Gentamicin (GM), an aminoglycoside antibiotic is one of the well know drugs/chemicals to cause nephrotoxicity both in humans and animals. A study on the effects of a synthetic phenolic compound, called 5-a, on GM-induced nephrotoxicity in male Wistar albino rats was conducted. The rats were grouped into five groups: normal control (NC), GM control (GM), positive control (GM + Dexa), treatment I (GM + 5-a 5 mg/kg) and treatment II (GM + 5-a 10 mg/kg). Throughout the experiment, the rats' weights were monitored, and at its conclusion, their serum and kidney tissues were analyzed for renal function indicators and inflammatory markers. The study also included histopathological evaluations, molecular docking studies, blood and urine analyses for electrolyte changes, and behavioural assessments for central nervous system impact. 2-{5-[(2-hydroxyethyl)-sulfanyl]-1,3,4-oxadiazol-2-yl} phenol (5-a) significantly protected against renal damage by reducing inflammatory markers, improving antioxidant defences, and decreasing kidney injury, particularly at higher doses. The findings suggest that compound 5-a, due to its anti-inflammatory and antioxidant properties, could be a promising therapeutic option for reducing gentamicin-induced nephrotoxicity and potentially for other kidney disorders in the future. These findings highlight the therapeutic effects of compound 5-a in alleviating gentamicin-induced nephrotoxicity.

Sections du résumé

BACKGROUND BACKGROUND
Nephrotoxicity, the rapid impairment of kidney function caused by harmful drugs and chemicals, affects about 20% of cases and is projected to become a leading cause of death by reactive oxygen species (ROS). Gentamicin (GM), an aminoglycoside antibiotic is one of the well know drugs/chemicals to cause nephrotoxicity both in humans and animals.
METHODS METHODS
A study on the effects of a synthetic phenolic compound, called 5-a, on GM-induced nephrotoxicity in male Wistar albino rats was conducted. The rats were grouped into five groups: normal control (NC), GM control (GM), positive control (GM + Dexa), treatment I (GM + 5-a 5 mg/kg) and treatment II (GM + 5-a 10 mg/kg). Throughout the experiment, the rats' weights were monitored, and at its conclusion, their serum and kidney tissues were analyzed for renal function indicators and inflammatory markers. The study also included histopathological evaluations, molecular docking studies, blood and urine analyses for electrolyte changes, and behavioural assessments for central nervous system impact.
RESULTS RESULTS
2-{5-[(2-hydroxyethyl)-sulfanyl]-1,3,4-oxadiazol-2-yl} phenol (5-a) significantly protected against renal damage by reducing inflammatory markers, improving antioxidant defences, and decreasing kidney injury, particularly at higher doses. The findings suggest that compound 5-a, due to its anti-inflammatory and antioxidant properties, could be a promising therapeutic option for reducing gentamicin-induced nephrotoxicity and potentially for other kidney disorders in the future.
CONCLUSION CONCLUSIONS
These findings highlight the therapeutic effects of compound 5-a in alleviating gentamicin-induced nephrotoxicity.

Identifiants

pubmed: 39334457
doi: 10.1186/s40360-024-00765-3
pii: 10.1186/s40360-024-00765-3
doi:

Substances chimiques

Gentamicins 0
Anti-Bacterial Agents 0
Antioxidants 0
Protective Agents 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

68

Informations de copyright

© 2024. The Author(s).

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Auteurs

Sony Amir (S)

Department of Pharmacy, Quaid-i-Azam University, Islamabad, Pakistan.

Muhammad Abid (M)

Department of Pharmacy, Quaid-i-Azam University, Islamabad, Pakistan.

Humaira Nadeem (H)

Riphah Institute of Pharmaceutical Sciences, Riphah International University, Islamabad, Pakistan.

Muhammad Khalid Tipu (MK)

Department of Pharmacy, Quaid-i-Azam University, Islamabad, Pakistan.

Nadeem Irshad (N)

Department of Pharmacy, Quaid-i-Azam University, Islamabad, Pakistan. nirshad@qau.edu.pk.

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