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. 2019 Apr 23;9:6432. doi: 10.1038/s41598-019-42933-0

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© The Author(s) 2019

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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CKD impairs adenosine monophosphate-activated protein kinase (AMPK) activation and promotes canonical NFκB activation. (A and B) Study of AMPK activation. (A) Representative images of the western blot analysis. (B) Quantitative data showing lower AMPK phosphorylation within ischemic hemispheres of CKD mice as compared to SHAM-operated mice. (C and D) Study of IκBα degradation. (C) Representative images of the western blot analysis. (D) Quantitative data showing lower IκBα expression within ischemic hemispheres of CKD mice as compared to SHAM-operated mice. (E and F) Study of p65 phosphorylation. (E) Representative images of the western blot analysis. (F) Quantitative data showing higher phosphorylation of P65 within ischemic hemispheres of CKD mice as compared to SHAM-operated mice. Results are expressed as mean ± SEM and represent data from 4 animals per group. *p < 0.05 CKD versus SHAM mice (non parametric Mann-Whitney U test). Ipsi: ipsilateral hemisphere. Raw western blot data are provided in Supplementary Figs 5, 6 and 7.