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. 2021 Aug 13;22(4):1175. doi: 10.3892/etm.2021.10607

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Copyright: © Yang et al.

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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AMPK mediates HG-induced filtration barrier injury of GEnCs. (A) Structure of PF. (B) Effect of HG on the permeability of GEnCs to FITC-dextran. (C) Western blot analysis of p-AMPKα (Thr-172) and total AMPK. (D) Densitometric analysis of AMPK, p-AMPKα (Thr-172) and the p-AMPKα (Thr-172)/AMPK ratio. (E) Effect of AICAR (1 mM) on the HG-induced permeability of GEnCs. (F) Representative images of glycocalyx staining with FITC-WGA. Data are presented as the mean ± standard deviation of three repeats. ^**P<0.01, ^***P<0.001 vs. control group; ^##P<0.01 vs. HG group. AMPK, adenosine monophosphate-activated protein kinase; HG, high glucose; GEnCs, glomerular endothelial cells; FITC, fluorescein isothiocyanate; p-, phosphorylated-; AICAR, 5-aminoimidizole-4-carboxamide riboside; WGA, wheat germ agglutinin.