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EA can activate ERK1/2 pathways and cyclin expression [119, 120] and neuroprotection can be obtained by proliferation of glial fibrillary acidic protein (GFAP)/vimentin/nestin-positive phenotypic astrocytes by enhancing BDNF expression in the peri-infarct cortex and striatum [121]

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The polarization of macrophages into M1 or M2 phenotypes is modulated by stimuli and signals from the inflammatory microenvironment [39]