Folic acid prevents cardiac dysfunction and reduces myocardial fibrosis in a mouse model of high-fat diet-induced obesity.
Folic acid prevents cardiac dysfunction and reduces myocardial fibrosis in a mouse model of high-fat diet-induced obesity.
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DOI：
10.1186/s12986-017-0224-0
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发表时间：
2017
影响因子：
4.5
通讯作者：
Wu J
中科院分区：
文献类型：
--
作者：
Li W;Tang R;Ouyang S;Ma F;Liu Z;Wu J
叶酸（FA）是一种抗氧化剂，可以减少活性氧的产生，并可以在缺血期间减轻心脏功能障碍。我们假设补充FA可以预防肥胖引起的心脏纤维化和心功能障碍。6周龄的C57 BL 6/J小鼠喂食高脂饮食（HFD）、正常饮食（ND）或补充有叶酸的HFD（FAD）14周。心功能测定采用经胸超声心动图exam. Phenotype分析包括测量体重和心脏重量，血糖和组织同型半胱氨酸（Hcy）含量，和心脏氧化应激状态。食用HFD会升高空腹血糖水平，导致肥胖和心脏扩大。在HFD喂养的小鼠中补充FA导致空腹血糖、心脏重量和心脏组织Hcy含量降低。我们还观察到当小鼠经受HFD喂养时显著的心脏收缩功能障碍，如左心室射血分数和缩短分数的降低所示。然而，FAD治疗改善了心脏功能。补充FA可防止HFD诱导的心脏纤维化。此外，HFD增加了心脏组织的丙二醛浓度，降低了抗氧化酶、谷胱甘肽和过氧化氢酶的水平。HFD消耗诱导心肌氧化应激，FA治疗可改善心肌氧化应激。FA补充显著降低小鼠血糖水平和心脏组织Hcy含量，并逆转HFD诱导的心功能障碍。这些心脏功能的改善可能通过减轻氧化应激和心肌纤维化来介导。
Folic acid (FA) is an antioxidant that can reduce reactive oxygen species generation and can blunt cardiac dysfunction during ischemia. We hypothesized that FA supplementation prevents cardiac fibrosis and cardiac dysfunction induced by obesity. Six-week-old C57BL6/J mice were fed a high-fat diet (HFD), normal diet (ND), or an HFD supplemented with folic acid (FAD) for 14 weeks. Cardiac function was measured using a transthoracic echocardiographic exam. Phenotypic analysis included measurements of body and heart weight, blood glucose and tissue homocysteine (Hcy) content, and heart oxidative stress status. HFD consumption elevated fasting blood glucose levels and caused obesity and heart enlargement. FA supplementation in HFD-fed mice resulted in reduced fasting blood glucose, heart weight, and heart tissue Hcy content. We also observed a significant cardiac systolic dysfunction when mice were subjected to HFD feeding as indicated by a reduction in the left ventricular ejection fraction and fractional shortening. However, FAD treatment improved cardiac function. FA supplementation protected against cardiac fibrosis induced by HFD. In addition, HFD increased malondialdehyde concentration of the heart tissue and reduced the levels of antioxidant enzyme, glutathione, and catalase. HFD consumption induced myocardial oxidant stress with amelioration by FA treatment. FA supplementation significantly lowers blood glucose levels and heart tissue Hcy content and reverses cardiac dysfunction induced by HFD in mice. These functional improvements of the heart may be mediated by the alleviation of oxidative stress and myocardial fibrosis.
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影响因子：
9.3
作者：
Mahajan, Rajiv;Lau, Dennis H.;Sanders, Prashanthan
通讯作者：
Sanders, Prashanthan
DOI：
10.1152/ajpheart.00475.2002
发表时间：
2002-12-01
影响因子：
4.8
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影响因子：
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影响因子：
120.7
作者：
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通讯作者：
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影响因子：
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作者：
Moens, An L.;Champion, Hunter C.;Kass, David A.
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