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. 2023 Nov 16;9:416. doi: 10.1038/s41420-023-01664-y

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© The Author(s) 2023

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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Fig. 1 — a Representative images of HepG2 and Hepa1-6 cells treated with 4 mM aspirin and control solution for 48 h. b CCK8 assays reveal cell growth curves of HepG2 and Hepa1-6 cells treated with 4 mM aspirin and control solution. c Representative images (left) and relative quantification (right) for the colony formation assays of HepG2 and Hepa1-6 cells with different treatments. d Representative micrographs (left) and relative quantification (right) for the EdU assays of HepG2 and Hepa1-6 cells with different treatments. e, f Cell cycle detection assays display the growth inhibition of aspirin on HepG2 and Hepa1-6 cells. g, h Cell apoptosis detection assays show the apoptosis induction of aspirin on HepG2 and Hepa1-6 cells. Error bars represent the means of three independent experiments. *P < 0.05, **P < 0.01, ***P < 0.001.