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. 2022 Jun 20;19:162. doi: 10.1186/s12974-022-02525-8

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© The Author(s) 2022

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 3 — Comparison of L5-VRT and SNI-induced expression of CX3CL1 in bilateral ACC. Representative protein microarray results (A) and the quantification analysis (B) showing that SNI triggered upregulations of chemokines CX3CL1 and CCL11 in contralateral ACC.*p < 0.05, **p < 0.01 versus sham group (n = 3 rats/group, one-way ANOVA). C, D Representative western blotting of CX3CL1 protein levels in bilateral ACC following SNI (C) and L5-VRT (D) are shown on the top and the quantification results are shown below. Significant differences are observed on the contralateral side in the SNI group but on the bilateral side in the L5-VRT group. *p < 0.05 versus sham group (n = 3 rats/group, one-way ANOVA)