ArticleJournal of biochemical and molecular toxicology2026
Hesperidin Attenuates Vincristine-Induced Nephrotoxicity via Nrf2/HO-1 and PI3K/Akt/mTOR Signaling.
Article in Journal of biochemical and molecular toxicology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Vincristine (VIN) is a widely used chemotherapeutic agent whose therapeutic application is substantially constrained by concentration-dependent toxicities, including nephrotoxicity. This study aimed to characterize the renoprotective capacity of hesperidin (HES) in a VIN-induced nephrotoxicity model and to delineate the mechanisms underlying its protective action. Twenty-eight female Wistar albino rats were divided into four groups: control, HES (200 mg/kg), VIN (0.17 mg/kg), and VIN (0.17 mg/kg) + HES (200 mg/kg), with all treatments administered for 7 consecutive days. Renal function markers, oxidative stress parameters, apoptosis- and autophagy-related gene expression, phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt)/mammalian target of rapamycin (mTOR) signaling components, and histopathological alterations were evaluated. VIN administration significantly increased serum urea and creatinine levels, lipid peroxidation, and oxidative DNA damage, while reducing antioxidant defenses (p < 0.05). VIN also induced marked apoptosis, evidenced by increased tumor protein p53 (p53), Bcl-2-associated X protein (Bax), Caspase-3, and C/EBP homologous protein (CHOP) expression and decreased B-cell lymphoma 2 (Bcl-2) levels, together with enhanced autophagy and suppression of PI3K/Akt/mTOR signaling (p < 0.05). These molecular changes were accompanied by severe renal histopathological damage (p < 0.05). HES supplementation significantly attenuated these effects by restoring antioxidant capacity, reducing inflammatory cytokines, suppressing apoptosis, modulating autophagy-related gene expression, and partially restoring PI3K/Akt/mTOR signaling (p < 0.05). Histopathological findings further confirmed the protective effect of HES against VIN-induced renal injury (p < 0.05). In conclusion, HES exerts renoprotective effects against VIN-induced nephrotoxicity by modulating interconnected oxidative stress, inflammation, apoptosis, autophagy, and PI3K/Akt/mTOR signaling pathways, suggesting its potential as a multi-target agent for preventing chemotherapy-associated renal injury in this experimental model.
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