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March 14, 2026Journal of Biochemical and Molecular Toxicology0 citationsOpen Access

Protective Effects of Hesperidin on Letrozole‐Induced Neurotoxicity: Involvement of Oxidative Stress, Apoptotic Signaling, and Inflammation

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İAİdris AyhanMKMunevver Nazlican KaplanDKDemet Dondu Kasim

Key Points

  • The study aims to understand letrozole's neurotoxic effects and assess the neuroprotective role of hesperidin.
  • Adult female rats were administered letrozole alone or with hesperidin over 4 weeks.
  • Biochemical analyses measured oxidant and antioxidant status, along with inflammatory markers.
  • Gene expression studies evaluated apoptotic signaling pathways.
  • Histopathological assessments examined brain tissue for damage.
  • Letrozole increased oxidative stress by elevating total oxidant status and reducing antioxidant status.
  • Pro-apoptotic gene Bax was upregulated, while anti-apoptotic gene Bcl-2 was downregulated in letrozole-treated rats.
  • Increased levels of pro-inflammatory markers IL-1, IL-6, TNF-α were observed alongside reduced IL-10 in response to letrozole.
  • Hesperidin co-treatment improved oxidative balance, normalized apoptotic gene expression, and decreased inflammation.

Abstract

ABSTRACT Letrozole, a widely used aromatase inhibitor for hormone receptor–positive breast cancer, has been suggested to be associated with potential neurotoxic effects; however, the underlying mechanisms remain unclear. This study aimed to investigate the neurotoxic effects of letrozole and evaluate the neuroprotective potential of hesperidin, a natural flavonoid with antioxidant and anti‐inflammatory properties. Adult female rats received letrozole alone or in combination with hesperidin for 4 weeks. Biochemical analyses showed that letrozole significantly increased total oxidant status (TOS) and decreased total antioxidant status (TAS), indicating oxidative stress. Gene expression results revealed upregulation of pro‐apoptotic Bax and downregulation of anti‐apoptotic Bcl 2 in letrozole‐treated rats, reflecting apoptotic activation. Additionally, inflammatory cytokine measurements demonstrated elevated pro‐inflammatory markers (IL‐1, IL‐6, TNF‐α) and reduced anti‐inflammatory IL‐10 following letrozole administration. Histopathological examination revealed cortical microhemorrhages, edema, and hyperemia. Importantly, co‐treatment with hesperidin attenuated oxidative imbalance, normalized apoptotic gene expression, modulated inflammatory cytokine levels towards an anti‐inflammatory profile, and ameliorated histological damage. These findings indicate that hesperidin confers neuroprotection by restoring redox balance, regulating apoptosis, and suppressing inflammation in letrozole‐induced neurotoxicity. Further studies are warranted to elucidate the precise molecular mechanisms and potential therapeutic applications of hesperidin in letrozole‐induced neurotoxicity.

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Cite This Study

Ayhan et al. (2026) studied this question.

synapsesocial.com/papers/69b4fc0eb39f7826a300c9e8https://doi.org/10.1002/jbt.70777
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