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. 2020 Apr 29;10:7283. doi: 10.1038/s41598-020-62984-y

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© The Author(s) 2020

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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Protective effect of E₁, E₂, and many of their endogenous metabolites against glutamate (GLU or G)-induced oxidative cell death in HT22 hippocampal neuronal cells. (a) The neuroprotective effect of E₁ and its metabolites (the inset is the structure of E₁). (b) The neuroprotective effect of E₂ and its metabolites (the inset is the structure of E₂). Cells are exposed to 5 mM glutamate for 24 h, and the estrogen (at three selected concentrations as shown) is introduced at the same time as glutamate. Note that cells in the control group are treated with vehicle only, whereas all other groups (including the estrogen groups) are treated with 5 mM glutamate. Cell viability is estimated using the MTT assay. Each value is mean ± S.D. of 6‒8 replicate measurements. *P < 0.05 versus the glutamate alone group.