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. 2021 Mar 23;12:649547. doi: 10.3389/fphys.2021.649547

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Copyright © 2021 Jia, Kang, Tan, Ren, Qu, Tang, Liu, Wang, Xiong and Yang.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Nicotinamide mononucleotide (NMN) administration before ischemia and during acute phase attenuated tubular DNA damage and cellular injury in uIRI mice at day 3 after surgery. (A) Schematic protocol of the experiments. (B) Representative images of HE (hematoxylin-eosin) staining and histologic analysis of tubular damage. Scale bars, 100 μm. (C) Quantification of damaged tubules of ischemic kidneys in (B). (D) Representative images of in situ TUNEL assay. Scale bars, 50 μm. (E) Quantification of apopotic tubular cells in ischemic kidneys in (D). (F) Western blots analysis of γH2A.X (ser139) showed decreased DNA damage in ischemic kidneys of NMN-treated mice compared with ischemic kidneys of PBS-treated mice. (G) Representative images of co-immunostaining of anti-Ki-67 and anti-p-H3 in kidney tissues. Scale bars, 50 μm. (H) Bar graphs showed no changes in number of Ki-67 positives tubular cells in NMN-treated mice, but a markedly reduction of tubular cells in G2/M phase compared with PBS-treated mice. n = 6–10/group. Data are means ± SD.