Pathological stresses such as pressure overload and myocardial infarction induce cardiac hypertrophy, which increases the risk of heart failure. Cacao bean polyphenols have recently gained considerable attention for their beneficial effects on cardiovascular diseases. This study investigated the effect of cacao bean polyphenols on the development of cardiac hypertrophy and heart failure. Cardiomyocytes from neonatal rats were pre-treated with cacao bean polyphenols and then stimulated with 30 µM phenylephrine. C57BL/6j male mice were subjected to sham or transverse aortic constriction surgery and then orally administered with vehicle or cacao bean polyphenols. Cardiac hypertrophy and function were examined by echocardiography. In cardiomyocytes, cacao bean polyphenols significantly suppressed phenylephrine-induced cardiomyocyte hypertrophy and hypertrophic gene transcription. Extracellular signal-regulated kinase 1/2 and GATA binding protein 4 phosphorylation induced by phenylephrine was inhibited by cacao bean polyphenols treatment in the cardiomyocytes. Cacao bean polyphenols treatment at 1200 mg/kg significantly ameliorated left ventricular posterior wall thickness, fractional shortening, hypertrophic gene transcription, cardiac hypertrophy, cardiac fibrosis, and extracellular signal-regulated kinase 1/2 phosphorylation induced by pressure overload. In conclusion, these findings suggest that cacao bean polyphenols prevent pressure overload-induced cardiac hypertrophy and systolic dysfunction by inhibiting the extracellular signal-regulated kinase 1/2-GATA binding protein 4 pathway in cardiomyocytes. Thus, cacao bean polyphenols may be useful for heart failure therapy in humans.

中文翻译：

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可可豆多酚抑制压力超负荷引起的心力衰竭模型小鼠的心脏肥大和收缩功能障碍

压力超负荷和心肌梗塞等病理应激会导致心脏肥大，从而增加心力衰竭的风险。可可豆多酚最近因其对心血管疾病的有益作用而备受关注。本研究调查了可可豆多酚对心脏肥大和心力衰竭发展的影响。新生大鼠的心肌细胞用可可豆多酚预处理，然后用 30 µM 去氧肾上腺素刺激。C57BL/6j 雄性小鼠接受假手术或横向主动脉缩窄手术，然后口服载体或可可豆多酚。通过超声心动图检查心脏肥大和功能。在心肌细胞中，可可豆多酚显着抑制去氧肾上腺素诱导的心肌细胞肥大和肥大基因转录。可可豆多酚处理可抑制去氧肾上腺素诱导的细胞外信号调节激酶 1/2 和 GATA 结合蛋白 4 磷酸化。1200 mg/kg 的可可豆多酚处理显着改善左心室后壁厚度、缩短分数、肥大基因转录、心脏肥大、心脏纤维化和压力超负荷诱导的细胞外信号调节激酶 1/2 磷酸化。综上所述，这些发现表明，可可豆多酚通过抑制心肌细胞中的细胞外信号调节激酶 1/2-GATA 结合蛋白 4 通路来预防压力超负荷引起的心脏肥大和收缩功能障碍。因此，可可豆多酚可用于治疗人类的心力衰竭。