Moreno Cristina, Macías Alvaro, Prieto Angela, de la Cruz Alicia, González Teresa, Valenzuela Carmen
Instituto de Investigaciones Biomédicas "Alberto Sols" (CSIC-UAM) Madrid, Spain.
Front Physiol. 2012 Jul 9;3:245. doi: 10.3389/fphys.2012.00245. eCollection 2012.
Dietary n-3 polyunsaturated fatty acids (PUFAs) have been reported to exhibit antiarrhythmic properties, and these effects have been attributed to their capability to modulate ion channels. In the present review, we will focus on the effects of PUFAs on a cardiac sodium channel (Na(v)1.5) and two potassium channels involved in cardiac atrial and ventricular repolarization (K(v)) (K(v)1.5 and K(v)11.1). n-3 PUFAs of marine (docosahexaenoic, DHA and eicosapentaenoic acid, EPA) and plant origin (alpha-linolenic acid, ALA) block K(v)1.5 and K(v)11.1 channels at physiological concentrations. Moreover, DHA and EPA decrease the expression levels of K(v)1.5, whereas ALA does not. DHA and EPA also decrease the magnitude of the currents elicited by the activation of Na(v)1.5 and calcium channels. These effects on sodium and calcium channels should theoretically shorten the cardiac action potential duration (APD), whereas the blocking actions of n-3 PUFAs on K(v) channels would be expected to produce a lengthening of cardiac action potential. Indeed, the effects of n-3 PUFAs on the cardiac APD and, therefore, on cardiac arrhythmias vary depending on the method of application, the animal model, and the underlying cardiac pathology.
据报道，膳食中的n-3多不饱和脂肪酸（PUFAs）具有抗心律失常特性，这些作用归因于它们调节离子通道的能力。在本综述中，我们将重点关注PUFAs对一种心脏钠通道（Na(v)1.5）以及参与心脏心房和心室复极化的两种钾通道（K(v)）（K(v)1.5和K(v)11.1）的影响。海洋来源的n-3 PUFAs（二十二碳六烯酸，DHA和二十碳五烯酸，EPA）以及植物来源的n-3 PUFAs（α-亚麻酸，ALA）在生理浓度下可阻断K(v)1.5和K(v)11.1通道。此外，DHA和EPA可降低K(v)1.5的表达水平，而ALA则不会。DHA和EPA还可降低由Na(v)1.5和钙通道激活所引发的电流幅度。理论上，这些对钠通道和钙通道的作用应会缩短心脏动作电位时程（APD），而n-3 PUFAs对K(v)通道的阻断作用预计会导致心脏动作电位延长。实际上，n-3 PUFAs对心脏APD以及因此对心律失常的影响会因应用方法、动物模型和潜在的心脏病理状况而有所不同。
