Harnessing electroacupuncture: a promising strategy against sleep deprivation-exacerbated post-cardiac arrest brain injury

Harnessing electroacupuncture: a promising strategy against sleep deprivation-exacerbated post-cardiac arrest brain injury

Abstract Cardiac arrest (CA)-induced post-cardiac arrest brain injury (PCABI) represents a critical contributor to global mortality and neurological disability. While sleep deprivation (SD) is recognized to aggravate neurological outcomes, its role in PCABI pathogenesis remains underexplored. This s...

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Bibliographic Details
Main Authors: Wenchao Fu, Cong Hu, Can Ma, Shihua Lv, Xianzhang Zeng, Tingting Li, Jiahui Chen, Xiao Han, Xin Tan, Xuefei Li, Wenzhi Li
Format: Article
Language:English
Published: Nature Portfolio 2025-08-01
Series:Scientific Reports
Subjects:
Cardiac arrest
Sleep deprivation
Electroacupuncture
Brain injury
EAAT2
Online Access:https://doi.org/10.1038/s41598-025-15563-y
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Summary:Abstract Cardiac arrest (CA)-induced post-cardiac arrest brain injury (PCABI) represents a critical contributor to global mortality and neurological disability. While sleep deprivation (SD) is recognized to aggravate neurological outcomes, its role in PCABI pathogenesis remains underexplored. This study investigated the mechanisms by which SD exacerbates PCABI and evaluated the neuroprotective efficacy of electroacupuncture (EA). A CA model was established in SD rats, followed by RNA sequencing and molecular analyses to assess brain injury biomarkers, synaptic plasticity, and calcium signaling pathways. SD disrupted circadian rhythms, amplified neuronal apoptosis, and suppressed glutamate transporter Excitatory Amino Acid Transporter 2 (EAAT2) expression post-CA, correlating with worsened cognitive deficits. EA treatment significantly attenuated these effects, restoring EAAT2 levels, mitigating calcium overload, and enhancing synaptic integrity. Mechanistically, EA modulated the EAAT2/calcium signaling axis and rebalanced autonomic nervous activity, thereby reducing oxidative stress and neuronal excitotoxicity. These findings identify EAAT2 downregulation as a key mediator of SD-aggravated PCABI and establish EA as a dual-target intervention that rectifies glutamatergic dysregulation and autonomic dysfunction. The study provides translational insights into EA’s therapeutic potential for PCABI, particularly in populations with comorbid sleep disturbances.
ISSN:2045-2322

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