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. 2017 Nov 27;7:16373. doi: 10.1038/s41598-017-16693-8

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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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The protective effect of minocycline on radiation-induced cell death in HT22 cells. (a) The colony formation of irradiated HT22 cells in the presence or absence of minocycline pretreatment. The data show that minocycline ameliorates the clonogenic inhibition of HT22 cells induced by X-irradiation. (b) Top panel: the representative histograms for Annexin V-FITC in cells treated with radiation and/or minocycline; Bottom panel: quantification of apoptosis in irradiated cells with and without minocycline at different times after radiation. Cells were collected at 48 and 72 h post IR, and assayed with Annexin V-FITC apoptosis detection kit. (c) Expression of cleaved caspase-3 in irradiated cells with and without minocycline 48 h (left panel) and 72 h (right panel) post IR. Total proteins were extracted from irradiated cells with and without minocycline at different times after radiation, then processed for immunoblotting as described in Materials and Methods. Cleaved caspase-3 and β-actin were probed from different parts of the same PVDF membrane. *P < 0.05, **P < 0.01 and ***P < 0.001 compared with the relative control.