400 Section - rTMS alleviates cerebral ischemia-reperfusion injury in rats: involvement of microglial M2 polarization and MerTK-mediated efferocytosis

Wednesday, May 20, 2026

6:00 PM - 7:30 PM PT

Presenting Author/Autor expositor(s)

YX

Yiyang Xiao, PhD

doctor
Department of Rehabilitation ，Rehabilitation Medicine Center ，Rehabilitation Laboratory， the First Affiliated Hospital ，Hengyang Medical School， University of South China
Hengyang, Hunan, China (People's Republic)

Co-Author/Coautor(s)

sL

shuzhi Y. Li, MS

doctor
Department of Rehabilitation ，Rehabilitation Medicine Center ，Rehabilitation Laboratory， the First Affiliated Hospital ，Hengyang Medical School， University of South China
Hengyang, Hunan, China (People's Republic)
HL

Huamin Li, MS

Physician
the First Affiliated Hospital of University of South China
Hengyang, Hunan, China (People's Republic)
xP

xingke Peng, MD

doctor
Department of Rehabilitation ，Rehabilitation Medicine Center ，Rehabilitation Laboratory， the First Affiliated Hospital ，Hengyang Medical School， University of South China
Hengyang, Hunan, China (People's Republic)
HT

Huali Tang, MS

None
Department of Rehabilitation ，Rehabilitation Medicine Center ，Rehabilitation Laboratory， the First Affiliated Hospital ，Hengyang Medical School， University of South China
Hengyang, Hunan, China (People's Republic)

Corresponding Author/Autor a quien dirigir la corr(s)

JZ

Jun Zhou, PhD

head of department
Rehabilitation department
Hengyang City, Hunan, China (People's Republic)

Objectives : This study established a middle cerebral artery occlusion (MCAO) model via the filament method to investigate whether the mechanism by which repetitive transcranial magnetic stimulation (rTMS) alleviates cerebral ischemia-reperfusion injury (CIRI) involves regulating microglial M2 polarization and MerTK-mediated efferocytosis, aiming to reveal a novel mechanism of rTMS against CIRI.

Design: Three-month-old male Sprague-Dawley rats were randomly divided into sham, model, and intervention groups (10 rats each). MCAO models were established in the model and intervention groups. The intervention group received rTMS treatment 24 hours post-modeling, once daily for 7 consecutive days. After modeling (sham and model groups) or completion of rTMS intervention (intervention group), neurological function scores were assessed. Brain tissues were collected for TTC staining (infarct volume), HE staining (histomorphology), and Nissl staining (neuronal damage). ELISA detected inflammatory factors and lactate levels in cerebrospinal fluid. Immunofluorescence co-localization of Iba1 (microglial marker) and MerTK was analyzed to calculate microglial efferocytosis efficiency. qRT-PCR and Western blot measured mRNA and protein levels of microglial polarization-related markers, MerTK, and efferocytosis pathway molecules (Gas6, Protein S) in the ischemic penumbra.

Results:

Compared to the sham group, the model group exhibited neurological deficits, increased cerebral infarct volume, severe cortical damage, elevated pro-inflammatory factors, decreased anti-inflammatory factors, upregulated M1 microglial polarization markers, downregulated M2 markers, reduced MerTK/Gas6/Protein S expression, and impaired microglial efferocytosis. After rTMS intervention, the intervention group showed alleviated neurological deficits, reduced infarct volume and cortical damage, decreased pro-inflammatory factors, increased anti-inflammatory factors, downregulated M1 markers, upregulated M2 markers, enhanced MerTK/Gas6/Protein S expression, and improved microglial efferocytosis compared to the model group.

Conclusion:

rTMS alleviates cerebral ischemia-reperfusion injury in rats by promoting microglial M2 polarization and enhancing MerTK-mediated efferocytosis.