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. 2022 Jan 29;28:11. doi: 10.1186/s10020-022-00442-3

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© The Author(s) 2022

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/.

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Fig. 9 — The mechanism by which eriodictyol inhibits AD. Eriodictyol alleviated cognitive injury by preventing neuronal ferroptosis, and its mechanism may be associated with VDR-mediated activation of Nrf2/HO-1 signaling. Eriodictyol up-regulated VDR expression and then activated the Nrf2/HO-1 signaling pathway by promoting the phosphorylation and nuclear translocation of Nrf2, thus regulating the expression of proteins related to ferroptosis