Arsenic toxicity is one of the major environmental problems causing various diseases, cardiovascular disorders is one of them. Several epidemiological studies have shown that arsenic causes cardiac hypertrophy but the detailed molecular mechanism is to be studied yet. This study is designed to determine the molecules involved in the augmentation of arsenic-induced cardiac hypertrophy. Furthermore, the effects of oleic acid on arsenic-induced hypertrophy and cardiac injury have also been investigated. Our results show that arsenic induces cardiac hypertrophy both in vivo in mice and in vitro in rat H9c2 cardiomyocytes. Moreover, arsenic results in decreased activity of AMPK and FoxO1 along with increased NFATc3 expression, a known cardiac hypertrophy inducer. In addition, activation of AMPK and FoxO1 results in reduced NFATc3 expression causing attenuation of arsenic-induced cardiac hypertrophy in H9c2 cells. Interestingly, we have observed that oleic acid helps in ameliorating cardiac hypertrophy in arsenic-exposed mice. Our studies on protection from arsenic-induced cardiac hypertrophy by oleic acid in H9c2 cells shows that oleic acid activates AMPK along with increased nuclear FoxO1 localization, thereby reducing NFATc3 expression and attenuating cardiomyocyte hypertrophy. This study will help in finding out new avenues in treating arsenic-induced cardiac hypertrophy.

中文翻译：

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油酸通过AMPK / FoxO / NFATc3途径保护免受砷诱导的心脏肥大。

砷毒性是引起各种疾病的主要环境问题之一，心血管疾病就是其中之一。几项流行病学研究表明，砷可引起心脏肥大，但详细的分子机制尚待研究。这项研究旨在确定参与砷诱导的心脏肥大的增加的分子。此外，还研究了油酸对砷引起的肥大和心脏损伤的影响。我们的结果表明，砷在小鼠体内和大鼠H9c2心肌细胞中均会诱发心脏肥大。此外，砷导致AMPK和FoxO1的活性降低，同时NFATc3表达增加，NFATc3是已知的心脏肥大诱导剂。此外，AMPK和FoxO1的激活导致NFATc3表达减少，从而导致砷诱导的H9c2细胞心肌肥大减弱。有趣的是，我们已经观察到油酸有助于缓解砷暴露小鼠的心脏肥大。我们关于油酸在H9c2细胞中免受砷诱导的心脏肥大的保护作用的研究表明，油酸激活AMPK并增加核FoxO1的定位，从而降低NFATc3的表达并减轻心肌肥大。这项研究将有助于寻找治疗砷引起的心脏肥大的新途径。我们关于油酸在H9c2细胞中免受砷诱导的心脏肥大的保护作用的研究表明，油酸激活AMPK并增加核FoxO1的定位，从而降低NFATc3的表达并减轻心肌肥大。这项研究将有助于寻找治疗砷引起的心脏肥大的新途径。我们关于油酸在H9c2细胞中免受砷诱导的心脏肥大的保护作用的研究表明，油酸激活AMPK并增加核FoxO1的定位，从而降低NFATc3的表达并减轻心肌肥大。这项研究将有助于寻找治疗砷引起的心脏肥大的新途径。