Fig. 8

A485 inhibits the H3K9bhb level of Lcn2 promoter and attenuates diabetic cardiomyopathy. A Illustration showing the inhibition of P300-mediated H3K9bhb by A485. B, C qRT-PCR and western blot analysis showing the mRNA (B) and protein (C) levels of LCN2 in H9C2 cells with Vehicle, PA or PA accompanied with A485 treatment. D, E Representative western blots (D) and immunostaining images (E) of H3K9bhb in H9C2 cells with Vehicle, PA or PA accompanied with A485 treatment. F ChIP analysis showing the H3K9bhb enrichment on the Lcn2 promoter in H9C2 cells with Vehicle, PA or PA accompanied with A485 treatment. G Schematic representation of the animal experiment workflow. H, I Representative left ventricular M-mode echocardiographic tracings, percentage of left ventricular ejection fraction (EF) and fractional shortening (FS) in the indicated mice. J, K Representative pulsed-wave Doppler tracings and ratio between mitral E wave and A wave (E/A) in the indicated mice. L, M qRT-PCR and western blot analysis showing the mRNA (L) and protein (M) levels of LCN2 in cardiac tissues from db/m or db/db mice with vehicle or A485 treatment. N Representative immunostaining images of H3K9bhb in cardiac tissues from db/m or db/db mice with vehicle or A485 treatment. O Representative images of H&E, Masson staining, immunohistochemistry staining of inflammatory factors and Tunel assay for heart sections from db/m or db/db mice with vehicle or A485 treatment. Bars: 500 μm in H&E; 100 μm in Masson staining, Tunel assay and immunohistochemistry staining. P, Q Quantification of fibrosis by assessing the Masson-positive areas (P) and apoptosis by counting the Tunel-positive cells (Q). n = 6 mice per group. All results are representative of three independent experiments. Values are presented as mean ± SD. *p < 0.05; **p < 0.01; ***p < 0.001