ArticleMolecular biology reports2025
The effect of hesperidin on trigeminal nerve damage in an NTG-induced migraine model: the role of the TRPV1 channel.
Article in Molecular biology reports, 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.
- Brain-derived neurotrophic factor via TRPM2 inhibition reduces amyloid-beta-mediated increases of apoptosis and mitochondrial oxidative neurotoxicity in neuronal cells.Metabolic brain disease · 2026Article
- TRPV1‑mediated central sensitisation: Core mechanisms of migraine chronification and novel targeted therapeutic strategies (Review).International journal of molecular medicine · 2026Review
- From bench to bedside: relevant animal models across the migraine attack phases.The journal of headache and pain · 2026Review
- A Review of the Effects of Herbal Medicines on the Conductance of Ion Channels.Physiological research · 2026Review
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMigraine is a common neurovascular disease associated with trigeminovascular activation and neurogenic inflammation. The transient receptor potential vanilloid-1 (TRPV1) channel plays a central role in nociceptive signalling, while hesperidin (HES), a citrus flavonoid, is known for its antioxidant and neuroprotective properties. This study evaluated the protective effects of HES on TRPV1-mediated pathways in the trigeminal nerve (TGN) in a nitroglycerin (NTG)-induced migraine model.
methodsC57BL/6j mice were randomly assigned to control, NTG, HES + NTG, capsazepine (CPZ) + NTG, and HES + CPZ + NTG groups. Migraine-like pain was induced with NTG (10 mg/kg, i.p.), while HES (200 mg/kg, gavage, 3 days) and CPZ (1 mg/kg, i.p.) were administered as treatments. Behavioral nociceptive assays (tail withdrawal, paw withdrawal, hot plate tests) were performed. The TGN was removed after the mice were killed sacrificed under anesthesia. Substance P, CGRP, BDNF, GSH, MDA, IL-1β, TNF-α, caspase-3, caspase-9, and TRPV1 levels in the TGN were analyzed by an ELISA kit. TRPV1 channel expression was measured in the TGN by western blot analysis. Also, TGN were evaluated histopathologically.
resultsNTG significantly induced hyperalgesia, oxidative stress, inflammatory cytokine release, apoptotic activation, and increased TRPV1. HES and CZP treatment significantly attenuated these changes, prolonging nociceptive thresholds, restoring antioxidant defences, suppressing neuropeptides, down-regulating TRPV1, and preserving neuronal morphology.
conclusionsHES treatment and TRPV1 channel inhibition offer a potential therapeutic opportunity for preventive and therapeutic strategies in the treatment of migraine.
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Registered trials
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