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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. 2. — Sodium dichloroacetate (DCA) attenuates ischemia-reperfusion (IR) injury in diabetic mice. (A) Hematoxylin and eosin (H&E) staining, periodic acid-Schiff (PAS) staining, neutrophil gelatinase-associated lipocalin (NGAL) staining, and kidney injury molecule-1 (KIM-1) staining of mice kidney tissues (original magnification ×200; scale bar, 100 μm; arrows, damaged tubules). (B) Serum blood urea nitrogen (BUN) and creatinine in mice. (C) Relative mRNA expression of pyruvate dehydrogenase kinase (Pdk) isoforms in mice kidney tissues. (D) Protein expression of PDK isoforms in mice kidney tissues. (E) Immunohistochemical image of p-pyruvate dehydrogenase E1α (p-PDHE1α) expression in mice kidney tissues (original magnification ×200; scale bar, 100 μm; arrow, positive regions). (F) Protein expression of p-PDHE1α in mice kidney. Data are the mean±standard error of the mean. STZ, streptozotocin. ^aP<0.01 vs. Control, ^bP<0.01 vs. STZ+IR, ^cP<0.01 vs. STZ, ^dP<0.05 vs. STZ+IR, ^eP<0.05 vs. STZ.