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. 2026 Feb 2;21:59. doi: 10.1186/s13020-026-01338-8

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© The Author(s) 2026

Open Access This 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 — EA mediated neuroinflammation by CXCR5. A EA suppressed the increase in ERK phosphorylation caused by IS. Mean ± SD. One-way ANOVA, R² = 0.8540. B, C IS significantly increased IL-6 and CCL2 mRNA expression, and EA treatment significantly decreased their up-regulation, but not by SEA. D EA suppressed the increase in ERK phosphorylation caused by AAV-CXCR5. Mean ± SD. One-way ANOVA, R² = 0.8775. E, F Overexpression of CXCR5 led to an increased elevation of IL-6 and CCL2 mRNA levels induced by IS, while silencing the CXCR5 gene can achieve the same inhibitory effect as EA. Mean ± SEM. One-way ANOVA. EA: electroacupuncture