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

Li,Qianxiao; Yu,Qin; Na,Rongmei; Liu,Baiting

doi:10.3892/etm.2017.5338

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

Authors:
- Qianxiao Li
- Qin Yu
- Rongmei Na
- Baiting Liu
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Affiliations: Department of Cardiology, Zhejiang Province Hospital of Integrated Traditional Chinese and Western Medicine, Hangzhou, Zhejiang 310003, P.R. China, Department of Cardiology, Affiliated Zhongshan Hospital of Dalian University, Dalian, Liaoning 116000, P.R. China
Published online on: October 18, 2017 https://doi.org/10.3892/etm.2017.5338
Pages: 6152-6158

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Abstract

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.

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