ArticleJournal of sleep research2025
Senegenin regulates the mechanism of insomnia through the Keap1/Nrf2/PINK1/Parkin pathway mediated by GAD67.
Article in Journal of sleep research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Oxidative stress in neurodegeneration: from a simple insult to a dynamic regulator.Redox report : communications in free radical research · 2026Review
- Umbilical Cord Mesenchymal Stem Cell-Derived Exosomes Alleviate Age-Related Insomnia in Rats by Suppressing Neuronal Ferroptosis in the Hippocampal Dentate Gyrus.Neurochemical research · 2026Article
- Hydrogen as a Potential Modulator: Implications for Mast Cell-Sleep-Wake Rhythm-Melatonin Interactions in Sleep Disorders.Molecular neurobiology · 2026Review
- Review
- Bioinformatics analysis of the mechanisms and efficacy of the Bushen Anzhi recipe in treating aging-related insomnia.Frontiers in psychiatry · 2026Article
- Senegenin regulates the mechanism of insomnia through the Keap1/Nrf2/PINK1/Parkin pathway mediated by GAD67.Journal of sleep research · 2025Article
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Abstract
GAD67 impacts insomnia as a key enzyme catalysing the conversion of glutamate (Glu) to gamma-aminobutyric acid (GABA). Senegenin enhances neuroprotection and is used widely to treat insomnia and other neurological diseases. This study aimed to investigate how senegenin regulates insomnia through a GAD67-mediated signalling pathway. We measured GAD67 expression levels in insomnia patients and evaluated the expression levels of GAD67 and Keap1/Nrf2/Parkin/PINK1-related cytokines following GAD67 lentiviral transfection in PC12 cells and in rat models. We also assessed cellular reactive oxygen species (ROS) and mitochondrial membrane potential levels. Additionally, EEG/EMG was used to analyse the sleep phases of rats and to assess memory and exploration functions. Pathological changes and the expression of GAD67 and sleep-related proteins in the hippocampus were examined. The results showed that GAD67 expression was increased in insomnia patients, ROS levels were elevated, and the mitochondrial membrane potential was decreased in the GAD67-KD group. Insomnia rats exhibited changes in sleep rhythm, learning, and exploration dysfunction, pathological changes in the CA1 region of the hippocampus, and differential expression of GAD67 and sleep-related factors. Inhibitory neurofactor expression levels were decreased in insomnia rats, showing a positive correlation in the GAD67-KD group and a negative correlation in the GAD67-OE group. Conversely, excitatory factor expression levels were increased in insomnia rats, showing a positive correlation in the GAD67-KD group and a negative correlation in the GAD67-OE group. Senegenin intervention modulated cytokine expression levels. In conclusion, GAD67 negatively regulates insomnia, and senegenin can regulate insomnia by mediating the expression of cytokines in the GAD67-regulated Keap1/Nrf2/Parkin/PINK1 pathway.
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