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. 2020 Jan 24;11:481. doi: 10.1038/s41467-020-14387-w

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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. 3 — a Superoxide was detected (as red fluorescence) in 3T3-L1 adipocytes treated with the control medium, or CM derived from proliferating young or replicative senescent EC. b Superoxide was detected in 3T3-L1 adipocytes treated with the control medium, or CM derived from control ECs (EC/GFP-CM) or premature senescent ECs (EC/TERF2DN-CM). c CDK inhibitor expression in 3T3-L1 adipocytes treated with the indicated EC-CM in the presence or absence of βNMN or NAC (n = 4 biologically independent samples each). A two-tailed Student’s t test was used for difference evaluation between the two groups. Data are presented as mean ± s.e. *P < 0.05, **P < 0.01, and ^#not significant. d SA-β-Gal staining in 3T3-L1 adipocytes treated with the indicated EC-CM in the presence or absence of βNMN or NAC. e Immunoblotting for the insulin signal pathway and IRS-1 in insulin-stimulated 3T3-L1 adipocytes treated with the indicated EC-CM in the presence or absence of βNMN or NAC. Bars: 100 μm. Source data are provided as a Source Data file.