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. 2020 Mar 30;6:17. doi: 10.1038/s41420-020-0252-9

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© The Author(s) 2020

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. 2 — a, b Atorvastatin induced senescence-associated β-galactosidase (SA-β-gal) activity in HepG2 and Hep3B cells. c, d Atorvastatin treatment of p53-wild-type HepG2 and p53-null Hep3B cells induced p21 and p27 expression but did not alter the expression of p14^ARF or p16^INK4a. HepG2 and Hep3B cells were treated with atorvastatin (0, 5, 10, or 20 μg/ml) for 72 h and then stained for SA-β-gal (a, b) and subjected to immunoblotting (c, d).