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Effects of a n-3 PUFA deficient diet on the expression of retinoid nuclear receptors,neurogranin and neuromodulin in rat brain

机译:n-3 PUFA缺乏饮食对大鼠脑中类维生素A核受体,神经氨酸和神经调节素表达的影响

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摘要

A lot of studies performed in rodents revealed that n-3 polyunsaturated fatty acid(PUFA)deficient diets could induce deficits of learning capacities but the mechanisms involved are not well known.Retinoic acid(RA)and its nuclear receptors(RAR and RXR)play a central role in the maintenance of cognitive processes and synaptic plasticity via its action on target genes that are neurogranin(RC3)and neuromodulin(CAP43).Given some interferences were described between the retinoid and fatty acid signaling pathways,we investigated the effects of a alpha-linolenic acid(18:3 n-3)deficient diet on retinoic acid nuclear receptors(RAR,and RXR),on QAP43 and RC3,and on blood and brain fatty acid composition in rats at three times of diet:3,9 and 18 weeks.In blood and brain of these animals,we observed a severe n-3 PUFA deficit(18:3 n-3,20:5 n-3 and particularly 22:6 n-3)associated with an increase in the n-6 PUFA content(mainly 22:5 n-6).Real-time PCR and western blot analysis allowed us to note that retinoid signaling,CAP43 and RC3 expression were affected in the striatum of the n-3 PUFA deprived rats.
机译:在啮齿动物上进行的大量研究表明,n-3多不饱和脂肪酸(PUFA)缺乏的饮食可能会导致学习能力的不足,但涉及的机制尚不清楚。视黄酸(RA)及其核受体(RAR和RXR)发挥通过其对目标基因神经颗粒(RC3)和神经调节蛋白(CAP43)的作用,在维持认知过程和突触可塑性中起着重要作用。鉴于类维生素A和脂肪酸信号通路之间存在一些干扰,我们研究了维生素A和脂肪酸信号通路之间的关系。三次饮食时大鼠的视黄酸核受体(RAR和RXR),QAP43和RC3以及大鼠血液和脑脂肪酸组成的α-亚麻酸(18:3 n-3)缺乏饮食:3,9和18周。在这些动物的血液和大脑中,我们观察到严重的n-3 PUFA缺乏症(18:3 n-3,20:5 n-3,尤其是22:6 n-3),与动物的血脂增加有关。 n-6 PUFA含量(主要是22:5 n-6)。实时PCR和Western blot分析使我们注意到维甲酸信号,CAP43和RC3的表达受到n-3 PUFA剥夺大鼠纹状体的影响。

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