Fig. 3

Chronic exposure to acrylamide exposure induces HF in mice. (A) Experimental design: 8-week-old mice exposed to acrylamide (0.5 mg/kg·bw per day) for 90 d. (B) The organ coefficient of the heart in control and acrylamide treatment groups. (C) Representative M-mode echocardiogram in control and acrylamide treatment groups. (D) Ejection fraction (%), (E) fractional shortening (%), (F) left ventricular internal dimension diastole (LVIDd) (in millimeters), and (G) left ventricular internal dimension systole (LVIDs) (in millimeters) based on echocardiogram results in control and acrylamide (AA) treatment groups (n = 5 per group). (H) Representative images of H&E and Masson staining of mouse heart sections in control and acrylamide treatment groups (0.5 mg/kg·bw per day). (I) Serum BNP level and (J) serum CK level in control and acrylamide treatment groups (n = 6 per group). (K to M) Relative mRNA expression of cardiac apoptosis-related genes and proteins in control and acrylamide-treated mice (n = 5 per group for quantitative polymerase chain reaction and n = 3 per group for Western blotting). (N) Relative mRNA expression of cardiac NOTCH and PI3K/AKT-related genes in control and acrylamide-treated mice (n = 5 per group). Data are presented as the means ± SEM. Significance was calculated using 2-tailed P values by unpaired Student’s t test; *P < 0.05, **P < 0.01, and ***P < 0.001.