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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. 2 — a Confocal analysis of the detection of 4-HNE-α-synuclein adducts (PL 4-HNE α-synuclein) in SNpc DA neurons of rats (Cohort 2). Rotenone treatment caused a significant accumulation of 4-HNE-α-synuclein adducts (red) in nigrostriatal neurons (TH, blue) that was inhibited in rats treated with 10-NO₂-OA (45 mg/Kg—Scale bar: 35 μm). b Quantification of PL 4-HNE-α-synuclein. Symbols represent the normalized means of the intensity (with Vehicle set at 100%) from a single rat (6 slices/brain). Statistical analysis was performed by one-way ANOVA with post hoc Bonferroni correction (*p < 0.0001 compared to Vehicle, ^#p < 0.0001 compared to Rotenone).