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. 2023 Mar 16;17:1105530. doi: 10.3389/fnins.2023.1105530

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Copyright © 2023 Lin, Liu, Song, Chen, Fu, Sun, Zhou, Bai, Wei and Li.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Upregulation of CXCL12 alleviated the spinal cord aberrations of experimental autoimmune encephalomyelitis (EAE) at the peak stage. At the peak stage of EAE, the significant differences in the glial fibrillary acidic protein (GFAP) and myelin basic protein (MBP) signals between the three groups showed that there was severe demyelination in the eGFP group and CXCL12-AMD3100 group. There were also significant differences in the CD45 and NG2 signals, suggesting that leukocyte infiltration likely led to deterioration of demyelination and that oligodendrocyte precursor cells (OPCs) were actively involved in remyelination. Data presented as the mean ± SEM. “*” represents value of P < 0.05, “**” represents value of P < 0.01, “***” represents value of P < 0.001 by two-tailed Student’s t-test or one-way ANOVA, n = 4–6 rats. The bar in the lower right represents 50 μm.