Research Paper Volume 15, Issue 22 pp 13384—13410

BDH1-mediated βOHB metabolism ameliorates diabetic kidney disease by activation of NRF2-mediated antioxidative pathway

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Figure 6. DM-Fumarate treatment reverses the Bdh1 deficiency-induced increase of renal inflammation and pathological injury. (AD) qRT-PCR analysis showing the IL-1β and IL-18 mRNA levels of indicated groups (5 μM DM-Fumarate for 48 h). (E) Representative WB image showing the protein level of BDH1 in the kidneys of WT and Bdh1-KO mice. (F) Urinary ACR values of mice in indicated groups (n = 3 in per group). (G) Representative photomicrographs of H&E, Masson, IHC (IL-1β), and TUNEL staining showing the pathological changes in the kidneys of indicated groups. All results are representative of three independent experiments. Values are presented as mean ± standard deviation. Bar: 50 μm in G. Abbreviations: ACR: albumin-to-creatinine ratio; Bdh1: β-hydroxybutyrate dehydrogenase 1; DKD: diabetic kidney disease; WB: western blot; H&E: hematoxylin and eosin; IHC: immunohistochemistry; STZ: streptozotocin; DM-Fumarate: dimethyl fumarate. *P < 0.05; **P < 0.01; ***P < 0.001; Abbreviation: ns: no significance.