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. 2023 Apr 7;9:55. doi: 10.1038/s41531-023-00502-3

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© The Author(s) 2023

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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 6 — a Rats treated with rotenone showed a significant increase in microglial activation (green) in SNpc analyzed immunohistochemically for the microglial activation marker, CD68 (red). Co-administration of 10-NO₂-OA (45 mg/Kg) inhibited rotenone-induced microglial activation (Scale bar main figure: 35 μm; Scale bar ×200 magnification: 15 μm). b Quantification of the signal relative to CD68 in microglia (Iba1) with symbols that represent the normalized means of the intensity (with Vehicle set at 100%) from a single rat (4 slices/brain). The number of animals per treatment group were the following: Vehicle (n = 7), 10-NO₂-OA (n = 9), Rotenone (n = 8), Rotenone + 10-NO₂-OA (n = 10). Statistical analysis was performed by one-way ANOVA with post hoc Bonferroni correction (*p < 0.0001 compared to Vehicle and 10-NO₂-OA, ^#p < 0.0001 compared to Rotenone).