Omega-3 polyunsaturated fatty acids prevent murine dilated cardiomyopathy by reducing oxidative stress and cardiomyocyte apoptosis.

Mice that lacked manganese-superoxide dismutase (Mn-SOD) activity exhibited the typical pathology of dilated cardiomyopathy (DCM). The aim of the present study was to investigate the effect of supplementation with omega-3 polyunsaturated fatty acids (n-3 PUFA) on heart function and oxidative stress biomarkers in mice with DCM. In the present study, heart/muscle-specific Mn-SOD-deficient mice (H/M-Sod2-/-) were treated with n-3 PUFA (30 mg/kg/day) for 10 weeks, and the reactive oxygen species (ROS) production in their heart mitochondria and cardiac function was subsequently assessed. n-3 PUFA treatment diminished ROS production and suppressed the progression of cardiac dysfunction. Furthermore, n-3 PUFA treatment effectively reversed the cardiac dysfunction and dilatation observed in symptomatic H/M-Sod2-/- mice. Notably, n-3 PUFA treatment ameliorated a molecular defect in connexin 43. Hematoxylin-eosin staining indicated that the phenotype of DCM was also ameliorated following n-3 PUFA treatment. Furthermore, echocardiography demonstrated that cardiac function was significantly improved in the mice treated with n-3 PUFA (P<0.05). Meanwhile, pre-treatment with n-3 PUFA significantly decreased cardiomyocyte apoptosis (P<0.001). In conclusion, n-3 PUFA treatment is able to prevent murine DCM, primarily by reducing ROS production and improving myocardial apoptosis. Therefore, the impairment of ROS production is proposed as a potential therapy for DCM.