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. 2018 Jan 29;8:1722. doi: 10.1038/s41598-018-20192-9

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© The Author(s) 2018

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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Induction of apoptosis by active compound 1i and VP-16 at the indicated concentrations on PC-3 cells. (a) 72 h after the treatment of these compounds at the indicated concentrations, cells were fixed, washed with PBS, stained with Hoechst 33258, and analyzed for morphological characteristics associated with apoptosis by fluorescence microscopic analysis (×20). (b) Compound 1i triggered changes of pro-caspase 3 and PARP by Western blotting analysis. Cells were lysed after 72 h treatment with 1i at the concentration (1, 2 and 4 μM). The lysates were resolved on a 10% SDS-PAGE, transferred on to a nitrocellulose membrane and probed for cleaved caspase 3 and PARP. β-actin was used as a loading control.