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. 2018 Jan 18;8:1055. doi: 10.1038/s41598-018-19573-x

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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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Over-expression of PLK1 partly rescues the apoptosis and proliferation inhibition caused by LPS in HT29 cells HT29 cells were transfected with pcDNA-PLK1-myc or the control cDNA for 24 h, then exposed to LPS (30 μg/ml) for 24 h. (A) A representative result of apoptosis analysed by Annexin V-FITC/PI double-labelling assay in HT29 cells after the above treatments. (B) Percentages of apoptotic cells in HT29 cells after the above treatments. Values are mean ± SEM (n = 3). **P < 0.01, ***P < 0.001. (C) The absorbance at 450 nm of HT29 cells after the above treatments. Values are mean ± SEM (n = 3). **P < 0.01, ***P < 0.001. (D) The levels of Ki67 and caspase3 after the above treatments. The graph represents the relative band densities. Values are mean ± SEM (n = 3). ***P < 0.001 versus control group. **P < 0.01 versus LPS group.