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Mechanistic pathways and in silico modeling of gallic acid- mediated protection against doxorubicin-induced nephrotoxicity in rats
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DOI：10.22038/ijbms.2026.90473.19500.png)
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Abstract
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Objective(s): This study aimed to evaluate the protective effects of Gallic acid (GA) against (Doxorubicin) DOX-induced renal injury and to explore potential molecular interactions underlying its effects. Materials and Methods: Fifty male rats were randomly assigned to five groups: Control, DOX, GA50+DOX, GA100+DOX, and GA100. DOX was administered as a single intraperitoneal dose on day 8 (40 mg/kg), while GA was given orally at 50 or 100 mg/kg for 10 consecutive days. Renal tissues were collected on day 11 and analyzed for oxidative stress markers, pro- and anti-inflammatory cytokines, and the apoptotic marker caspase-3 via ELISA. Immunohistochemistry assessed Nrf-2 and HO-1 expression, and histopathology evaluated structural alterations. Molecular docking simulations were performed for DOX/topoisomerase II alpha (PDB ID: 4FM9) and GA/TNF-alpha (PDB ID: 2AZ5). Results: GA significantly ameliorated DOX-induced oxidative stress, inflammatory cytokine imbalance, caspase-3 activation, and histological damage in a dose-dependent manner, while enhancing Nrf-2 and HO-1 expression. Docking analysis confirmed DOX binding to topoisomerase II alpha and revealed strong GA-TNF-alpha binding affinity. Conclusion: GA exerts substantial renoprotective effects against DOX-induced nephrotoxicity by modulating oxidative, inflammatory, and apoptotic pathways. The agreement between in vivo findings and in silico modeling supports GA as a potential complementary agent to reduce chemotherapyrelated renal injury.
Keywords:
Apoptosis
Doxorubicin
Gallic acid
Inflammation
Molecular docking
Nephrotoxicity Oxidative stress
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