ArticleMolecular neurobiology2025
The Potential Protective Effects of Intermittent Fasting Against Radiation-Induced Brain Damage in a Rat Model: Suggested Involvement of IRS-1/PI3 K/AKT and BDNF/TrkB Signaling Pathways.
Article in Molecular neurobiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Interplay Between Autophagy, Cellular Senescence, and Brain Aging: Neuroprotective Implications of Intermittent Fasting.Cellular and molecular neurobiology · 2026Review
- Time-Restricted Feeding Preserves Synaptic Function and Modulates Reelin andJournal of nutrition and metabolism · 2026Article
- Friend or Foe: Dietary Restriction and Its Protective Effects on Responses to Ionizing Radiation.Dose-response : a publication of International Hormesis SocietyReview
- Research Progress on Dietary Intervention in Radiation Protection.Dose-response : a publication of International Hormesis SocietyReview
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fasting has emerged as a promising therapeutic strategy for neurological disorders, offering protection against insults such as ionizing radiation (IR), which can cause irreversible brain damage. Intermittent fasting (IF), including alternate-day fasting (ADF) and time-restricted feeding (TRF), is being explored for its neuroprotective effects with potential involvement of key signaling pathways such as IRS-1/PI3K/AKT and BDNF/TrkB. Thirty-six male Wistar albino rats were randomly divided into six groups: normal feeding (NF, ad libitum feeding), ADF, TRF (6-h feeding window), NF plus radiation (NF-irradiated, 20-Gy cranial exposure), ADF plus radiation (ADF-irradiated), and TRF plus radiation (TRF-irradiated). Oxidative stress markers, antioxidant enzymes, liver and kidney function parameters, and gene/protein expression levels (IRS1, AKT1, PI3K, GFAP, 8-OHdG, BDNF, TrkB) were evaluated using enzyme-linked immunosorbent assay (ELISA) and RT-PCR, complemented by histopathological analysis. IR significantly impaired antioxidant defenses (GSH, GST, CAT), suppressed IRS-1/PI3K/AKT and BDNF/TrkB signaling, and elevated oxidative damage markers (MDA, ROS, 8-OHdG), inflammation (GFAP), and markers of organ dysfunction (ALT, AST, GGT, urea, creatinine). Both IF regimens mitigated these effects; however, TRF demonstrated greater efficacy than ADF. TRF more effectively reduced oxidative stress, improved antioxidant enzyme activity, and more robustly restored metabolic and neurotrophic signaling pathways. Both ADF and TRF provided neuroprotection against radiation-induced brain injury, but TRF exhibited superior outcomes in reducing oxidative stress and preserving neuronal integrity. These findings highlight TRF as a potentially more effective dietary strategy for mitigating radiation-induced neurotoxicity, with possible contributions from the modulation of IRS-1/PI3K/AKT and BDNF/TrkB pathways.
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