Fig. 1: Rnd3 expression was markedly downregulated in DIC. | Cell Death & Disease

Fig. 1: Rnd3 expression was markedly downregulated in DIC.

From: Rnd3 protects against doxorubicin-induced cardiotoxicity through inhibition of PANoptosis in a Rock1/Drp1/mitochondrial fission-dependent manner

Fig. 1

A Schematic diagram depicting the experimental strategy. B Representative M-mode echocardiographic images of the left ventricle in mice received Saline or Dox. C Left ventricular ejection fraction (LVEF) assessed by echocardiography (n = 12). D, E The serum levels of cardiac LDH and CK-MB were significantly elevated in the Dox-treated WT mice compared to the WT mice using ELISA (n = 8). F Kaplan-Meier survival analysis showing deceased survival in Dox-treated WT mice compared with WT mice (n = 12). G Volcano plot for differential gene expression in the Dox-treated WT mice compared to the WT mice, P-value < 0.05. H Cardiac Rnd3 protein level was evaluated from the indicated treatment groups at 0,1, 2 and 4 weeks following Dox treatment. I Quantitative analysis of Rnd3 protein expression (n = 8). J Quantitative analysis of Rnd3 mRNA expression (n = 8). K Representative images of immunohistochemical staining of Rnd3 from mice heart in control groups and Dox groups (yellow arrow), Scale bar = 40 μm. L Quantitation of immunohistochemical staining of the Rnd3-positive area of (K) (n = 8). M Representative images of immunofluorescence staining of Rnd3 (green) in cardiomyocytes (red), Scale bar = 40 μm. cTnT were employed as markers for cardiomyocytes. N Quantitative analysis of mean Rnd3 fluorescence intensity (n = 8). Data were presented as mean ± SD. Student’s t-test was used for statistical analysis in (C)–(F), (I), (J), (L), and (N).

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