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. 2022 Mar 4;13:94. doi: 10.1186/s13287-022-02754-x

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© The Author(s) 2022

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. 4 — MSCs dose-dependently protect L-O2 cells from APAP-induced necrosis. a Giemsa staining of the surviving L-O2 cells after treatment with NAC (6 mM) or co-culture with different numbers of MSCs (5 × 10⁵, 1 × 10⁶, 1.5 × 10⁶, 2 × 10⁶ cells) in the presence of APAP (20 mM). b Annexin V and 7-AAD staining and flow cytometry analysis showed that MSCs dose-dependently increased the proportion of surviving L-O2 cells in the presence of APAP (20 mM), and the survival rate of L-O2 cells co-cultured with 2 × 10⁶ MSCs was similar to that of the cells treated with NAC (6 mM)