Pain research & management · 2026
Transcranial Photobiomodulation Attenuates Neurogenic Inflammation and Sensory Hypersensitivity in a Nitroglycerin-Induced Migraine Model: Toward a Nonpharmacological Therapy.
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Kazmi Sareh, Vatandoust Seyed Mahdi, Athari Seyed Zanyar, Ebrahimian Asal, Moradi Afshin, Mahmoudi Javad, Sadigh-Eteghad Saeed, Rajabi Mojgan, Akhbari-Shojaei Sina, Neshan-Alipour Ramtin, Nozad Abdollah, Hosseinkhani Moein, Hosseini Leila, Hamblin Michael R, Farajdokht Fereshteh
Аннотация
BACKGROUND: Migraine is a debilitating neurological condition, characterized by headache, photophobia, and heightened mechanical/thermal sensitivity. Current pharmacological therapies often lead to incomplete relief and adverse effects, necessitating the use of noninvasive alternatives. This study evaluated transcranial photobiomodulation (PBM) in a nitroglycerin (NTG)-induced migraine model in male mice.
METHODS: Mice were assigned to Sham, NTG, NTG + Sumatriptan (SUMA; 600 µg/kg, s.c.), NTG + PBM, and NTG + PBM + SUMA groups. Over 9 days, NTG (5 mg/kg) was injected intraperitoneally every other day to develop an animal model of chronic migraine. The PBM protocol involved daily irradiation (810 nm) on the occipital bone of the head for 5 s over 9 days. The animals underwent behavioral testing for photophobia, mechanical allodynia, and thermal sensitivity. The trigeminal nucleus caudalis (TNC) was assessed for miR-155 expression by real-time PCR and protein expression of phospho-NF-κB, IL-1β, transient receptor potential ankyrin 1 (TRPA1) and vanilloid 1 (TRPV1), calcitonin gene-related peptide (CGRP), c-Fos, and pituitary adenylate cyclase-activating polypeptide (PACAP) using immunoblotting.
RESULTS: Behavioral assessment revealed that PBM significantly reduced head scratching and improved exploratory activity, decreased light aversion, reversed periorbital/hindpaw mechanical allodynia, and prolonged thermal withdrawal latency compared to the NTG group. Moreover, PBM downregulated miR-155 expression and decreased levels of inflammatory mediators and migraine-associated neuropeptides in the TNC. Notably, combined PBM and SUMA treatment resulted in improvements in behavioral and molecular outcomes compared to either treatment alone.
CONCLUSION: These results indicate that PBM inhibited migraine-like behaviors and decreased the expression of numerous molecular markers that are linked to neuroinflammation and trigeminal activation in the TNC. These findings establish a foundation for additional research on transcranial PBM as a noninvasive method for modulating migraine-related behavioral responses.
METHODS: Mice were assigned to Sham, NTG, NTG + Sumatriptan (SUMA; 600 µg/kg, s.c.), NTG + PBM, and NTG + PBM + SUMA groups. Over 9 days, NTG (5 mg/kg) was injected intraperitoneally every other day to develop an animal model of chronic migraine. The PBM protocol involved daily irradiation (810 nm) on the occipital bone of the head for 5 s over 9 days. The animals underwent behavioral testing for photophobia, mechanical allodynia, and thermal sensitivity. The trigeminal nucleus caudalis (TNC) was assessed for miR-155 expression by real-time PCR and protein expression of phospho-NF-κB, IL-1β, transient receptor potential ankyrin 1 (TRPA1) and vanilloid 1 (TRPV1), calcitonin gene-related peptide (CGRP), c-Fos, and pituitary adenylate cyclase-activating polypeptide (PACAP) using immunoblotting.
RESULTS: Behavioral assessment revealed that PBM significantly reduced head scratching and improved exploratory activity, decreased light aversion, reversed periorbital/hindpaw mechanical allodynia, and prolonged thermal withdrawal latency compared to the NTG group. Moreover, PBM downregulated miR-155 expression and decreased levels of inflammatory mediators and migraine-associated neuropeptides in the TNC. Notably, combined PBM and SUMA treatment resulted in improvements in behavioral and molecular outcomes compared to either treatment alone.
CONCLUSION: These results indicate that PBM inhibited migraine-like behaviors and decreased the expression of numerous molecular markers that are linked to neuroinflammation and trigeminal activation in the TNC. These findings establish a foundation for additional research on transcranial PBM as a noninvasive method for modulating migraine-related behavioral responses.