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膳食多不饱和脂肪酸可改变心肌蛋白激酶C的表达,并影响慢性缺氧诱导的心脏保护作用。

Dietary polyunsaturated fatty acids alter myocardial protein kinase C expression and affect cardioprotection induced by chronic hypoxia.

作者信息

Hlavácková Markéta, Neckár Jan, Jezková Jana, Balková Patricie, Stanková Barbora, Nováková Olga, Kolár Frantisek, Novák Frantisek

机构信息

Charles University, Faculty of Science, Department of Biochemistry, Hlavova 8, 128 43 Prague 2, Czech Republic.

出版信息

Exp Biol Med (Maywood). 2007 Jun;232(6):823-32.

PMID:17526775
Abstract

We examined the influence of dietary fatty acid (FA) classes on the expression of protein kinase C (PKC) delta and epsilon in relation to the cardioprotective effects of chronic intermittent hypoxia (CIH). Adult male Wistar rats were fed a nonfat diet enriched with 10% lard (saturated FA [SFA]), fish oil (n-3 polyunsaturated FA [n-3 PUFA]), or corn oil (n-6 PUFA) for 10 weeks. After 4 weeks on the diet, each group was divided into two subgroups that were either exposed to CIH in a barochamber (7000 m, 8 hrs/ day) or kept at normoxia for an additional 5-6 weeks. A FA phospholipid profile and Western blot analysis of PKC were performed in left ventricles. Infarct size was assessed in anesthetized animals subjected to 20-min coronary artery occlusion and 3-hr reperfusion. CIH decreased the n-6/n-3 PUFA ratio in all groups by 23% independently of the initial value set by various diets. The combination of n-3 diet and CIH had a stronger antiarrhythmic effect during reperfusion than the n-3 diet alone; this effect was less pronounced in rats fed the n-6 diet. The normoxic n-6 group exhibited smaller infarctions (by 22%) than the n-3 group. CIH decreased the infarct size in n-3 and SFA groups (by 20% and 23%, respectively) but not in the n-6 group. Unlike PKC epsilon, the abundance of PKC delta in the myocardial particulate fraction was increased by CIH except for the n-6 group. Myocardial infarct size was negatively correlated (r=- 0.79) with the abundance of PKC delta in the particulate fraction. We conclude that lipid diets modify the infarct size-limiting effect of CIH by a mechanism that involves the PKC delta-dependent pathway.

摘要

我们研究了膳食脂肪酸(FA)类别对蛋白激酶C(PKC)δ和ε表达的影响,以及其与慢性间歇性缺氧(CIH)心脏保护作用的关系。成年雄性Wistar大鼠喂食富含10%猪油(饱和脂肪酸[SFA])、鱼油(n-3多不饱和脂肪酸[n-3 PUFA])或玉米油(n-6 PUFA)的无脂饮食10周。饮食4周后,每组分为两个亚组,一组在气压舱中暴露于CIH(7000米,每天8小时),另一组在常氧环境下再维持5 - 6周。对左心室进行FA磷脂谱分析和PKC的蛋白质印迹分析。在接受20分钟冠状动脉闭塞和3小时再灌注的麻醉动物中评估梗死面积。CIH使所有组的n-6/n-3 PUFA比值降低23%,与各种饮食设定的初始值无关。n-3饮食与CIH联合在再灌注期间比单独的n-3饮食具有更强的抗心律失常作用;这种作用在喂食n-6饮食的大鼠中不太明显。常氧n-6组的梗死面积比n-3组小(22%)。CIH使n-3和SFA组的梗死面积减小(分别为20%和23%),但n-6组没有。与PKCε不同,除n-6组外,CIH使心肌微粒体部分中PKCδ的丰度增加。心肌梗死面积与微粒体部分中PKCδ的丰度呈负相关(r = -0.79)。我们得出结论,脂质饮食通过涉及PKCδ依赖性途径的机制改变CIH的梗死面积限制作用。

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