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. 2024 Feb 1;48(3):405–417. doi: 10.4093/dmj.2023.0196

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Copyright © 2024 Korean Diabetes Association

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Fig. 1. — Pyruvate dehydrogenase kinase 4 (PDK4) is induced in ischemia-reperfusion (IR) kidney injury in diabetic mice. (A) Hematoxylin and eosin (H&E) staining in mouse kidneys (original magnification ×200; scale bar, 100 μm; arrows, damaged tubules). (B) Relative mRNA level of Pdk isoforms in mice kidney tissues. (C) Protein expression and quantitative graph of PDK isoforms in mice kidney tissues. (D) Immunohistochemical image of p-pyruvate dehydrogenase E1α (p-PDHE1α) expression in mice kidney tissues (original magnification: ×200; scale bar, 100 μm; arrow, positive regions). (E) Protein expression and quantitative graph of p-PDHE1α in mice kidney tissues. Data are the mean±standard error of the mean. STZ, streptozotocin. ^aP<0.01 vs. Control, ^bP< 0.05, ^cP<0.01, ^dP<0.001 vs. STZ.