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. 2021 Dec 12;8:61. doi: 10.1186/s40779-021-00355-y

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© The Author(s) 2021

Open AccessThis 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 2 — Effect of melatonin on DNA damage and apoptosis of postradiation CBSCs. a Analysis of DNA breaks using γH2AX immunostaining. DAPI (blue) and γH2AX (red). b Analysis of apoptosis by flow cytometry. c Levels of anti-apoptotic protein BCL-2 and pro-apoptotic protein BAX were measured by Western blotting. Compared with control, ^*P < 0.05; compared with IR, ^#P < 0.05. IR irradiation, IR + LMLT irradiation plus low 1 μmol/L melatonin treatment, IR + MMLT irradiation plus medium 10 μmol/L melatonin treatment, IR + HMLT irradiation plus high 100 μmol/L melatonin treatment, CBSCs cortical bone-derived stem cells, γH2AX gamma H2A histone family member X, BCL-2 B-cell lymphoma-2, BAX BCL2-associated X