CNS neuroscience & therapeutics · 2025
Study on the Mechanisms of Ischemic Stroke Impacting Sleep Homeostasis and Circadian Rhythms in Rats.
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Chu Ting-Ting, Sun Chen, Zheng Yong-Hui, Gao Wen-Ying, Zhao Lin-Lin, Zhang Jing-Yu
Аннотация
OBJECTIVE: This study aimed to investigate the impact of ischemic stroke (IS) on sleep homeostasis and circadian rhythms in rats, as well as the underlying mechanisms.
METHODS: The middle cerebral artery occlusion model was employed to induce IS in rats. Sixty young and sixty aged rats were randomly divided into six groups for experiments. Neurological function was assessed using the Garcia score, and infarct size was evaluated through 2,3,5-triphenyltetrazolium chloride staining. Sleep-wake cycles were monitored by implanting electrodes into the neck muscles to record electroencephalograms and electromyograms. Parameters such as sleep latency, waking time, non-rapid eye movement (NREM) sleeping, rapid eye movement sleeping, NREM delta power, and waking theta power were measured. Serum cortisol and melatonin levels were measured using enzyme-linked immunosorbent assay. Gene and protein expression of circadian regulators period 1 (Per1) and cryptochrome 1 (Cry1) in the pineal gland were assessed using real-time quantitative reverse transcription polymerase chain reaction and western blot.
RESULTS: Compared to the sham groups, IS-induced rats showed a decrease in Garcia scores and an increase in cerebral infarction area. Besides, relative to young rats, aged rats exhibited more severe cerebral infraction damage, lower melatonin levels, higher cortisol levels, disrupted sleep-wake cycles, and altered gene and protein expression levels of Per1 and Cry1 in the pineal gland.
CONCLUSIONS: IS can lead to neurological impairments and brain damage, with aged rats showing more severe effects. IS also disturbs melatonin and cortisol levels, affects sleep homeostasis, and results in disordered Per1 and Cry1 gene and protein expression levels. These findings underscore the role of circadian disruption and stress response in the pathology of IS, especially in aging populations.
METHODS: The middle cerebral artery occlusion model was employed to induce IS in rats. Sixty young and sixty aged rats were randomly divided into six groups for experiments. Neurological function was assessed using the Garcia score, and infarct size was evaluated through 2,3,5-triphenyltetrazolium chloride staining. Sleep-wake cycles were monitored by implanting electrodes into the neck muscles to record electroencephalograms and electromyograms. Parameters such as sleep latency, waking time, non-rapid eye movement (NREM) sleeping, rapid eye movement sleeping, NREM delta power, and waking theta power were measured. Serum cortisol and melatonin levels were measured using enzyme-linked immunosorbent assay. Gene and protein expression of circadian regulators period 1 (Per1) and cryptochrome 1 (Cry1) in the pineal gland were assessed using real-time quantitative reverse transcription polymerase chain reaction and western blot.
RESULTS: Compared to the sham groups, IS-induced rats showed a decrease in Garcia scores and an increase in cerebral infarction area. Besides, relative to young rats, aged rats exhibited more severe cerebral infraction damage, lower melatonin levels, higher cortisol levels, disrupted sleep-wake cycles, and altered gene and protein expression levels of Per1 and Cry1 in the pineal gland.
CONCLUSIONS: IS can lead to neurological impairments and brain damage, with aged rats showing more severe effects. IS also disturbs melatonin and cortisol levels, affects sleep homeostasis, and results in disordered Per1 and Cry1 gene and protein expression levels. These findings underscore the role of circadian disruption and stress response in the pathology of IS, especially in aging populations.