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首页> 外文期刊>Life sciences >Effects of docosahexaenoic acid on calcium pathway in adult rat cardiomyocytes.
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Effects of docosahexaenoic acid on calcium pathway in adult rat cardiomyocytes.

机译：二十二碳六烯酸对成年大鼠心肌细胞钙途径的影响。

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摘要

In this study we examined the effect of polyunsaturated fatty acids (PUFAs), in particular of docosahexaenoic acid (DHA), on calcium homeostasis in isolated adult rat cardiomyocytes exposed to KCl, ET-1 and anoxia. Free [Ca(2+)](i) in rat cardiomyocytes was 135.7 +/- 0.5 nM. Exposure to 50 mM KCl or 100 nM ET-1 resulted in a rise in free [Ca(2+)](i) in freshly isolated cells (465.4 +/- 15.6 nM and 311.3 +/- 12.6 nM, respectively) and in cultured cells (450.8 +/- 14.8 nM and 323.5 +/- 14.8 nM respectively). An acute treatment (20 minutes) with 10 microM DHA significantly reduced the KCl- and ET-1-induced [Ca(2+)](i) increase (300.9 +/- 18.1 nM and 232.08 +/- 11.8 nM, respectively). This reduction was greater after chronic treatment with DHA (72 h; 257.7 +/- 13.08 nM and 192.18 +/- 9.8 nM, respectively). Rat cardiomyocytes exposed to a 20 minute superfusion with anoxic solution, obtained by replacing O(2) with N(2) in gas mixture, showed a massive increase in cytosolic calcium (1200.2 +/- 50.2 nM). Longer exposure to anoxia induced hypercontraction and later death of rat cardiomyocytes. Preincubation with DHA reduced the anoxic effect on [Ca(2+)](i) (498.4 +/- 7.3 nM in acute and 200.2 +/- 12.2 nM in chronic treatment). In anoxic conditions 50 mM KCl and 100 nM ET-1 produced extreme and unmeasurable increases of [Ca(2+)](i.) Preincubation for 20 minutes with DHA reduced this phenomenon (856.1 +/- 20.3 nM and 782.3 +/- 7.6 nM, respectively). This reduction is more evident after a chronic treatment with DHA (257.7 +/- 10.6 nM and 232.2 +/- 12.5 nM, respectively). We conclude that in rat cardiomyocytes KCl, ET-1 and anoxia interfered with intracellular calcium concentrations by either modifying calcium levels or impairing calcium homeostasis. Acute, and especially chronic, DHA administration markedly reduced the damage induced by calcium overload in those cells.
机译：在这项研究中，我们研究了多不饱和脂肪酸（PUFA），尤其是二十二碳六烯酸（DHA）对暴露于KCl，ET-1和缺氧的成年大鼠心肌细胞钙稳态的影响。大鼠心肌细胞中的游离[Ca（2 +）]（i）为135.7 +/- 0.5 nM。暴露于50 mM KCl或100 nM ET-1导致新鲜分离的细胞（分别为465.4 +/- 15.6 nM和311.3 +/- 12.6 nM）中的游离[Ca（2 +）]（i）升高。培养的细胞（分别为450.8 +/- 14.8 nM和323.5 +/- 14.8 nM）。急性治疗（20分钟）用10 microM DHA显着降低了KCl-和ET-1诱导的[Ca（2 +）]（i）升高（分别为300.9 +/- 18.1 nM和232.08 +/- 11.8 nM） 。长期接受DHA治疗后，这种减少更大（分别为72小时; 257.7 +/- 13.08 nM和192.18 +/- 9.8 nM）。大鼠心肌细胞暴露于缺氧溶液20分钟超融合，通过用混合气体中的N（2）代替O（2）获得，显示出胞质钙的大量增加（1200.2 +/- 50.2 nM）。长时间暴露于缺氧会导致过度收缩，并随后导致大鼠心肌细胞死亡。与DHA的预孵育降低了对[Ca（2 +）]（i）的缺氧作用（急性治疗为498.4 +/- 7.3 nM，慢性治疗为200.2 +/- 12.2 nM）。在缺氧条件下，50 mM KCl和100 nM ET-1产生[Ca（2 +）]（i。）极端且不可测量的增加。用DHA预孵育20分钟可减少这种现象（856.1 +/- 20.3 nM和782.3 +/-分别为7.6 nM）。在长期接受DHA治疗后（分别为257.7 +/- 10.6 nM和232.2 +/- 12.5 nM），这种减少更为明显。我们得出的结论是，在大鼠心肌细胞中，KCl，ET-1和缺氧症通过改变钙水平或损害钙稳态来干扰细胞内钙浓度。急性（尤其是长期的）DHA给药显着减少了这些细胞中钙超载引起的损伤。

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