{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,17]],"date-time":"2026-09-17T16:37:47Z","timestamp":1789663067896,"version":"4.0.1"},"reference-count":29,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2024,6,10]],"date-time":"2024-06-10T00:00:00Z","timestamp":1717977600000},"content-version":"vor","delay-in-days":9,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/100019558","name":"Qingdao Key Health Discipline Development Fund","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100019558","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J of Neuroscience Research"],"published-print":{"date-parts":[[2024,6]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    Neuroinflammation caused by excessive microglial activation plays a key role in the pathogenesis of ischemic stroke. Repetitive transcranial magnetic stimulation (rTMS) is a noninvasive neuromodulatory technique that has recently been reported to regulate microglial functions and exert anti\u2010inflammatory effects. The intermittent burst stimulation (iTBS) regimen in rTMS improves neuronal excitability. However, whether iTBS exerts its anti\u2010inflammatory effects by stimulating neurons and thereby modulating microglial polarization remains unclear. Motor function was assessed after 1\u2009week of rTMS (iTBS regimen) treatment in adult male mice with occlusion\/reperfusion of the middle cerebral artery (MCAO\/r) injury. We also investigated the molecular biological alterations associated with microglial polarization using a cell proliferation assay, multiplex cytokine bioassays, and immunofluorescence staining. iTBS regimen can improve balance and motor coordination function, increase spontaneous movement, and improve walking function in mice with early cerebral ischemia injury. Expression levels of IL\u20101\u03b2, TNF\u2010\u03b1, and IL\u201010 increased significantly in mice with MCAO injury. Especially, rTMS significantly increased the number of proliferating cells in the infarcted cortex. The fluorescence intensity of MAP2 in the peri\u2010infarct area of MCAO injured mice was low, but the signal was broader. Compared with MCAO group, the fluorescence intensity of MAP2 in rTMS group was significantly increased. rTMS inhibited pro\u2010inflammatory M1 activation (Iba1\n                    <jats:sup>+<\/jats:sup>\n                    \/CD86\n                    <jats:sup>+<\/jats:sup>\n                    ) and improved anti\u2010inflammatory M2 activation (Iba1\n                    <jats:sup>+<\/jats:sup>\n                    \/CD206\n                    <jats:sup>+<\/jats:sup>\n                    ) in the peri\u2010infarct zone, thus significantly changing the phenotypic ratio M1\/M2. rTMS improves motor dysfunction and neuroinflammation after cerebral I\/R injury in mice by regulating microglial polarization.\n                  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