Fig. 2

BDH1 deficiency aggravates diabetes-induced cardiac dysfunction in vivo and palmitic acid-induced cardiomyocyte injury in vitro. Schematic representation of the animal experiment workflow. B Representative immunoblotting images of BDH1 protein levels in the cardiac tissues from db/m; WT, db/m; Bdh1−/−, db/db; WT and db/db; Bdh1−/− mice. C Representative left ventricular M-mode echocardiographic tracings, percentage of left ventricular ejection fraction (EF) and fractional shortening (FS) in the indicated mice. D Representative pulsed-wave Doppler tracings and ratio between mitral E wave and A wave (E/A) in the indicated mice. E Representative images of H&E, Masson staining, Tunel assay and immunohistochemistry staining of inflammatory factors for heart sections from indicated mice. Bars: 1 mm in H&E; 100 μm in Masson staining and Tunel assay; 200 μm in immunohistochemistry staining. F, G Quantification of fibrosis by assessing the Masson-positive areas (F) and apoptosis by counting the Tunel-positive cells (G) in the heart sections from indicated mice. n = 6 mice per group. H Representative immunoblotting images of BDH1 expression in H9C2 cells transfected with control siRNA (siNC) or Bdh1 targeted siRNA (siBdh1). I, J Representative immunoblotting images of inflammatory factors and cleaved caspase 3 in siNC- or siBdh1-transfected H9C2 cells with or without PA treatment. K mRNA expression of inflammatory factors in siNC- or siBdh1-transfected H9C2 cells with or without PA treatment. L, M Tunel assay showing the apoptosis level of siNC- or siBdh1-transfected H9C2 cells (L) and primary cardiomyocytes isolated from fetal WT or Bdh1−/− mice (M) with PA treatment. n = 3 repeated experiments in H-M. Values are presented as mean ± SD. *P < 0.05; **P < 0.01; ***P < 0.001