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孕期补充胆碱可减轻胎儿期低蛋白饮食对子代大鼠空间学习能力缺陷的影响。

Prenatal choline supplementation attenuates spatial learning deficits of offspring rats exposed to low-protein diet during fetal period.

机构信息

School of Public Health, Sun Yat-sen University, Guangzhou 510080, People's Republic of China.

出版信息

J Nutr Biochem. 2016 Jun;32:163-70. doi: 10.1016/j.jnutbio.2015.09.003. Epub 2015 Sep 13.

Abstract

Prenatal intake of choline has been reported to lead to enhanced cognitive function in offspring, but little is known about the effects on spatial learning deficits. The present study examined the effects of prenatal choline supplementation on developmental low-protein exposure and its potential mechanisms. Pregnant female rats were fed either a normal or low-protein diet containing sufficient choline (1.1g/kg choline chloride) or supplemented choline (5.0g/kg choline chloride) until delivery. The Barnes maze test was performed at postnatal days 31-37. Choline and its metabolites, the synaptic structural parameters of the CA1 region in the brain of the newborn rat, were measured. The Barnes maze test demonstrated that prenatal low-protein pups had significantly greater error scale values, hole deviation scores, strategy scores and spatial search strategy and had lesser random search strategy values than normal protein pups (all P<.05). These alterations were significantly reversed by choline supplementation. Choline supplementation increased the brain levels of choline, betaine, phosphatidylethanolamine and phosphatidylcholine of newborns by 51.35% (P<.05), 33.33% (P<.001), 28.68% (P<.01) and 23.58% (P<.05), respectively, compared with the LPD group. Prenatal choline supplementation reversed the increased width of the synaptic cleft (P<.05) and decreased the curvature of the synaptic interface (P<.05) induced by a low-protein diet. Prenatal choline supplementation could attenuate the spatial learning deficits caused by prenatal protein malnutrition by increasing brain choline, betaine and phospholipids and by influencing the hippocampus structure.

摘要

产前摄入胆碱已被报道可导致后代认知功能增强,但对于空间学习缺陷的影响知之甚少。本研究探讨了产前补充胆碱对发育性低蛋白暴露的影响及其潜在机制。妊娠雌性大鼠在整个孕期给予正常或低蛋白饮食(含足够胆碱(1.1g/kg 氯化胆碱)或补充胆碱(5.0g/kg 氯化胆碱))直至分娩。在出生后第 31-37 天进行 Barnes 迷宫测试。测量了胆碱及其代谢物、新生大鼠大脑 CA1 区的突触结构参数。 Barnes 迷宫测试表明,产前低蛋白仔鼠的错误尺度值、洞偏离分数、策略分数和空间搜索策略显著高于正常蛋白仔鼠(均 P<.05),随机搜索策略值显著降低(均 P<.05)。这些改变通过补充胆碱得到显著逆转。补充胆碱可使新生仔鼠大脑中的胆碱、甜菜碱、磷脂酰乙醇胺和磷脂酰胆碱水平分别增加 51.35%(P<.05)、33.33%(P<.001)、28.68%(P<.01)和 23.58%(P<.05),与 LPD 组相比。产前补充胆碱可逆转低蛋白饮食引起的突触间隙宽度增加(P<.05)和突触界面曲率减小(P<.05)。产前补充胆碱可通过增加大脑中的胆碱、甜菜碱和磷脂来减轻产前蛋白质营养不良引起的空间学习缺陷,并影响海马结构。

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