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Peer-reviewedCC BYJournal of biochemical and molecular toxicology

Hesperidin Attenuates Vincristine-Induced Nephrotoxicity via Nrf2/HO-1 and PI3K/Akt/mTOR Signaling.

  • Aydin Genc1
  • Bayram Akoglan2
  • Emre Sahin2,3
  • Eren Cankaya4
4 affiliations
  1. 1Department of Biochemistry, Faculty of Veterinary Medicine, Bingol University, Bingol, Türkiye.
  2. 2Animal Nutrition and Nutritional Disease Department, Faculty of Veterinary Medicine, Bingol University, Bingol, Türkiye.
  3. 3Department of Veterinary Biostatistics, Health Sciences Institute, Ankara University, Ankara, Türkiye.
  4. 4Department of Pathology, Faculty of Veterinary Medicine, Firat University, Elazig, Turkey.
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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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Cite

BibTeXRIS
BibTeX
@article{genc2026hesperidin,
  title = {{Hesperidin Attenuates Vincristine-Induced Nephrotoxicity via Nrf2/HO-1 and PI3K/Akt/mTOR Signaling.}},
  author = {Aydin Genc and Bayram Akoglan and Emre Sahin and Eren Cankaya},
  journal = {Journal of biochemical and molecular toxicology},
  year = {2026},
  month = oct,
  doi = {10.1002/jbt.71136},
  url = {https://europepmc.org/article/MED/42893422},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - Hesperidin Attenuates Vincristine-Induced Nephrotoxicity via Nrf2/HO-1 and PI3K/Akt/mTOR Signaling.
AU  - Aydin Genc
AU  - Bayram Akoglan
AU  - Emre Sahin
AU  - Eren Cankaya
PY  - 2026
DA  - 2026/10/30
JO  - Journal of biochemical and molecular toxicology
DO  - 10.1002/jbt.71136
UR  - https://europepmc.org/article/MED/42893422
AB  - 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.
SN  - 1095-6670
SN  - 1099-0461
ER  -