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. 2023 Mar 29;20:86. doi: 10.1186/s12974-023-02762-5

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© The Author(s) 2023

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. 9 — Effect of nicotinic acid (NA) on midbrain dopaminergic neuron damage and striatal dopamine levels in LPS-injected mice in the presence or absence of HCA2 on microglia. A Mouse handling flowchart. B, C The number of TH-positive cells in the substantia nigra (SN) of the mouse midbrain, as detected by immunohistochemistry (the bar represents 50 μm). D, E TH protein in mouse midbrain, as detected using the western blotting method. F, G The levels of dopamine and its metabolites (DOPAC) in mouse striatum, as detected by HPLC technique. Results are presented as mean ± SD (n = 3). *p < 0.05, **p < 0.01, ***p < 0.00 means significant difference