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Oxidative Stress and Mitophagy in Rats With Nitroglycerin/Inflammatory Soup-Induced Migraine: A Comparative Study
Wen-Xiu Sun1, Ting-Yan Chen1, Mao-Mei Song1
1Department of Neurology, Headache Center, The First Hospital of Shanxi Medical University, Taiyuan, 030001, Shanxi, China, sxmu.edu.cn.
Pain Research & Management
|April 1, 2026
Summary
Nitroglycerin and interictal sensitization models both increase oxidative stress and decrease mitophagy in rats, contributing to migraine susceptibility. These findings highlight the role of mitochondrial dysfunction in migraine pathogenesis.
Area of Science:
- Neuroscience
- Mitochondrial Biology
- Pathophysiology
Background:
- Oxidative stress and mitochondrial dysfunction are implicated in migraine.
- Reduced mitophagy exacerbates mitochondrial damage and cellular stress.
- Mitochondrial dysfunction may increase migraine susceptibility, but comparative studies are lacking.
Purpose of the Study:
- To comparatively investigate the roles of oxidative stress and mitophagy in nitroglycerin (NTG)- and interictal sensitization (IS)-induced migraine models in rats.
Main Methods:
- Male Sprague-Dawley rats were assigned to control, NTG, or IS groups.
- Migraine-like behaviors, mechanical thresholds, and oxidative stress markers were assessed.
- Mitophagy markers (PINK1, Parkin, LC3II/I) and mitochondrial proteins were quantified.
Main Results:
- Both NTG and IS models reduced mechanical thresholds, with NTG causing more pronounced head scratching and freezing.
- NTG elevated malondialdehyde and depleted glutathione/superoxide dismutase; IS primarily reduced superoxide dismutase.
- Both models showed decreased LC3II/I ratio and reduced PINK1 and Parkin expression, indicating impaired mitophagy.
Conclusions:
- NTG and IS administration comparably reduced mechanical thresholds and increased oxidative stress.
- Both migraine models demonstrated decreased mitophagy in the trigeminal nucleus caudalis.
- These findings underscore the link between oxidative stress, mitophagy impairment, and migraine pathogenesis.
