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. 2018 Feb 6;8:2477. doi: 10.1038/s41598-018-20821-3

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© The Author(s) 2018

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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Effects of ROCK inhibitors on insulin action and signaling. (A) 3T3-L1 cells were differentiated through incubation in DM (without insulin) with KD025, Y-27632, or fasudil, as previously indicated, and stained with Oil Red O on day 8. (B) Lipid accumulation was assessed by measuring the absorbance at 520 nm of Oil Red O. ***p < 0.001 vs. DM control. (C,D) 3T3-L1 cells were differentiated in DMI-containing media with or without KD025 for 2, 4, or 8 days. (C) Cells lysates were subjected to SDS-PAGE and immunoblotted with anti-phospho-Akt (Ser473) and total Akt antibodies. PPARγ was used as a differentiation marker, and β-tubulin and α-actin as loading controls. (D) The level of phosphorylated Akt at Ser473 residue was illustrated during adipogenesis. *p < 0.05; **p < 0.01; ***p < 0.001 vs. insulin + vehicle untreated. The data are the representative from more than three independent experiments. Data are expressed as means ± S.E. based on triplicate.