Ellagic acid confers protection against gentamicin-induced oxidative damage, mitochondrial dysfunction and

Mohammad Reza Sepand1, Mohammad Hossein Ghahremani1, Kamal Razavi-Azarkhiavi2

  • 1Department of Pharmacology and Toxicology, Faculty of Pharmacy, Tehran University of Medical Sciences, Tehran, Iran.

Abstract

Insights

Ellagic acid (EA) protects against gentamicin (GEN)-induced kidney damage by reducing oxidative stress and apoptosis. This study demonstrates EA

Area of Science:

  • Pharmacology
  • Toxicology
  • Biochemistry

Background:

  • Gentamicin (GEN) is an antibiotic known to cause nephrotoxicity.
  • Oxidative stress and apoptosis are key mechanisms in GEN-induced kidney injury.

Purpose of the Study:

  • To evaluate the protective effects of ellagic acid (EA) against gentamicin-induced nephrotoxicity.
  • To explore the underlying biochemical, molecular, and histopathological mechanisms of EA's action.

Main Methods:

  • Rats were divided into control, GEN, EA, and GEN + EA groups for 10 days.
  • Biochemical markers (creatinine, urea), oxidative stress markers, and apoptotic markers were assessed.
  • Kidney tissues were analyzed using histopathology and molecular techniques.

Main Results:

  • EA significantly reduced plasma creatinine and urea levels in GEN-treated rats.
  • EA ameliorated oxidative stress by normalizing lipid peroxidation, antioxidant enzyme activity (CAT, SOD), and glutathione levels.
  • EA exhibited anti-apoptotic effects by modulating caspase-3 activation and Bcl-2/Bax expression, and protected mitochondria from GEN-induced damage.

Conclusions:

  • Ellagic acid demonstrates significant nephroprotective effects against gentamicin toxicity in rats.
  • These protective effects are attributed to the antioxidant and anti-apoptotic properties of EA.

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