Effects of intermittent theta burst stimulation on the inflammatory response and cerebral blood flow in promoting neurovascular repair after ischemic stroke

Abstract Secondary injuries from ischemia‒reperfusion in stroke, such as edema and hemorrhagic transformation, can significantly impact brain function. This study investigated the effects of intermittent theta burst stimulation (iTBS) on neurological function and cerebral blood flow in a mouse model...

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Main Authors: Jingjun Zhang, Siyue Li, Dan Huang, Jiale Fu, Shuying Chen, Na Ren, Pengkun Yang, Di Song, Xiaochen Bai, Hongyu Xie, Gang Liu, Kewei Yu, Shamay S. M. Ng, Junfa Wu, Xiao Xiao, Yi Wu
Format: Article
Language:English
Published: BMC 2025-06-01
Series:Molecular Brain
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Online Access:https://doi.org/10.1186/s13041-025-01222-w
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Summary:Abstract Secondary injuries from ischemia‒reperfusion in stroke, such as edema and hemorrhagic transformation, can significantly impact brain function. This study investigated the effects of intermittent theta burst stimulation (iTBS) on neurological function and cerebral blood flow in a mouse model of ischemia‒reperfusion injury. Laser speckle flowmetry was used to assess changes in cortical blood flow before and after ischemia‒reperfusion. Behavioral assessments were conducted to evaluate motor function recovery. The impact of iTBS on neuronal damage and apoptosis in the peri-infarct area was evaluated via Nissl staining and a TUNEL assay. RNA transcriptome sequencing and immunofluorescence staining were performed to investigate the effects of iTBS on microglial and astrocyte activation and the associated inflammatory response. Our findings demonstrated that iTBS significantly mitigated abnormal perfusion in the infarcted hemisphere, reduced neuronal damage and apoptosis in the peri-infarct area, and enhanced motor function in ischemic mice. Furthermore, iTBS promoted the polarization of microglia and astrocytes toward the anti-inflammatory M2 and A2 phenotypes. Therefore, iTBS provides neurovascular protection by modulating microglial and astrocyte activation and regulating the inflammatory response in the peri-infarct area, thereby improving abnormal cerebral blood flow in both the acute and subacute phases after ischemic brain injury.
ISSN:1756-6606