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. 2017 Aug 23;7:9209. doi: 10.1038/s41598-017-08957-0

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© The Author(s) 2017

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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Involvement of the PI3K/Akt pathway in the neuroprotective effect of CE. (A,B and C) Cell lysates were analysed by immunoblotting to measure the relative levels of proteins involved in the Akt signalling pathway, including phosphorylated (Ser473) Akt and its downstream target Bcl-2 (A). Quantification of p-Akt and Bcl-2 protein levels is shown in (B and C), respectively. (D) Cell viability was measured using the MTT assay. In this experiment, cells were pretreated with the Akt inhibitor LY29004 for 30 min prior to treatment with CE or glutamate. (E and F) Immunoblot showing the Bcl-2 protein level (E); the intensity of the bands in each lane was quantified (F). (B,C and F), n = 3; D, n = 5; data are shown as mean ± SEM; One-way ANOVA followed by Tukey’s multiple comparisons test. **p < 0.01, ***p < 0.001.