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. 2019 Apr 3;9:5585. doi: 10.1038/s41598-019-42088-y

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© The Author(s) 2019

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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Quantification of immunohistochemistry studies. (A) Histological images representing hematoxylin and eosin staining for morphology of tumor (1^st row), immunohistochemistry images of Ki-67 for cellular proliferation (2^nd row), and TUNEL staining for DNA damage (3^rd row) for control, NTX, and TMZ group, respectively. Scale bar is 100 µm in ×200. (B) Significantly decreased expression of Ki-67 reflects the decreased cell proliferation in NTX-treated animals (P = 0.0209) compared with the control. The Ki-67 expression was significantly increased in TMZ-treated mice (P = 0.0209) compared to that in NTX-treated mice. No significant difference was observed between control and TMZ-treated mice. (C) Significantly increased TUNEL positive cells reflects the increased DNA damage in NTX-treated animals (P = 0.0209) compared with that in the control animals. No significant changes in DNA damage were observed between untreated and TMZ-treated mice (P = 0.5637) or NTX and TMZ-treated mice (P = 0.2482). Data are represented as median with an interquartile range of four independent experiments.