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. 2023 Feb 11;13:2452. doi: 10.1038/s41598-023-29287-4

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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 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/.

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(A–F) This figure shows the relative expression of α-synuclein, TH, p-Trk B, BDNF, p-CREB, in which β-actin acts as a control (A). The lower expression of BDNF (B), p-Trk B (C), CREB (D), TH (E) was observed in case of rotenone-intoxicated mice (***p < 0.001) (**p < 0.01) respectively. while OLE administered group showed significantly increased expression of TH, CREB, BDNF and p-Trk B and BDNF (***p < 0.001) (**p < 0.01) respectively. Aggregation of α-synuclein (F) was found to be more in rotenone group (***p < 0.001) than control whereas OLE-treated group showed lower aggregation of α-synuclein (***p < 0.001). The one-way ANOVA was used to analyse the data, followed by the Newman–Keuls test. The mean ± SEM (n = 6) is used to depict the values.