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<p>Gentamicin (GEN) causes liver and kidney toxicity by generating free radicals and inflammation. This study tested gallic acid (GA) as an antioxidant to reduce this oxidative stress. Thirty-five male rats were divided into five groups: sham, GEN, and three GEN + GA groups with doses of 60, 90, and 120 mg/kg. After 10 days, the rats were euthanized, and their serum, kidneys, and livers were analyzed. Results showed that GEN significantly increased serum BUN, creatinine, AST, ALT, and ALP (<i>p</i> &lt; 0.05). It also raised malondialdehyde (MDA) levels and the expression of TNF-α and caspase-3 genes, with notable histopathological injuries in the kidneys and liver (<i>p</i> &lt; 0.05). GA demonstrated potential protective effects against GEN-induced damage. GEN reduced antioxidant enzyme activities (GPX, CAT, and GSH) in the organs (<i>p</i> &lt; 0.05). Conversely, GA at all doses lowered BUN, creatinine, ALT, AST, ALP, and MDA levels and decreased TNF-α and caspase-3 gene expression in the liver and kidneys (<i>p</i> &lt; 0.05). It also protected against tissue injuries and boosted antioxidant enzyme levels in both organs (<i>p</i> &lt; 0.05). The study shows that gallic acid (60, 90, 120 mg/kg) significantly mitigates gentamicin-induced hepatorenal toxicity by reducing oxidative stress, inflammation, and apoptosis. Notably, doses of 90 and 120 mg/kg were especially more effective in minimizing tissue damage and improving antioxidant activity.</p> Graphical Abstract <p></p>

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Effect of gallic acid in mitigating hepatorenal injuries induced by gentamicin administration in male Wistar rats

  • 期刊论文

  • 发表日期：

    2025年6月28日

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  • Mohammad Mehdi Behvandi,
  • Susan Sabbagh,
  • Reza Rostami,
  • Ayat Moradipour,
  • Marzieh Karami,
  • Ashkan Jafarian,
  • Marjan Jafarian,
  • Leila Jafaripour,
  • Reza Norouzirad

摘要

Gentamicin (GEN) causes liver and kidney toxicity by generating free radicals and inflammation. This study tested gallic acid (GA) as an antioxidant to reduce this oxidative stress. Thirty-five male rats were divided into five groups: sham, GEN, and three GEN + GA groups with doses of 60, 90, and 120 mg/kg. After 10 days, the rats were euthanized, and their serum, kidneys, and livers were analyzed. Results showed that GEN significantly increased serum BUN, creatinine, AST, ALT, and ALP (p < 0.05). It also raised malondialdehyde (MDA) levels and the expression of TNF-α and caspase-3 genes, with notable histopathological injuries in the kidneys and liver (p < 0.05). GA demonstrated potential protective effects against GEN-induced damage. GEN reduced antioxidant enzyme activities (GPX, CAT, and GSH) in the organs (p < 0.05). Conversely, GA at all doses lowered BUN, creatinine, ALT, AST, ALP, and MDA levels and decreased TNF-α and caspase-3 gene expression in the liver and kidneys (p < 0.05). It also protected against tissue injuries and boosted antioxidant enzyme levels in both organs (p < 0.05). The study shows that gallic acid (60, 90, 120 mg/kg) significantly mitigates gentamicin-induced hepatorenal toxicity by reducing oxidative stress, inflammation, and apoptosis. Notably, doses of 90 and 120 mg/kg were especially more effective in minimizing tissue damage and improving antioxidant activity.

Graphical Abstract