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孕期和产后酒精暴露诱导大鼠脑内神经退行性变的研究:甜菜碱和/或ω-3的保护作用

The investigation of the prenatal and postnatal alcohol exposure-induced neurodegeneration in rat brain: protection by betaine and/or omega-3.

作者信息

Kusat Ol Kevser, Kanbak Güngör, Oğlakcı Ilhan Ayşegül, Burukoglu Dilek, Yücel Ferruh

机构信息

Department of Biochemistry, Faculty of Medicine, University of Eskisehir Osmangazi, 26480, Eskisehir, Turkey.

Department of Anatomy, Faculty of Medicine, University of Eskisehir Osmangazi, Eskisehir, Turkey.

出版信息

Childs Nerv Syst. 2016 Mar;32(3):467-74. doi: 10.1007/s00381-015-2990-1. Epub 2016 Jan 5.

Abstract

PURPOSE

We aim to study the effect of neurodegeneration on the brain of rat pups caused by prenatal and postnatal ethanol exposure with modified liquid diet to elucidate protective effects of betaine and omega-3 supplementation. When ethanol is consumed during prenatal and postnatal periods, it may result in fetal alcohol syndrome (FAS) in the offspring.

METHODS

Rats were divided into control, ethanol, ethanol + betaine, ethanol + omega-3, ethanol + omega-3 + betaine groups. The effect of betaine and omega-3 in response to ethanol-induced changes on the brain, by biochemical analyses cytochrome c, caspase-3, calpain, cathepsin B and L, DNA fragmentation, histological and morfometric methods were evaluated.

RESULTS

Caspase-3, calpain, cathepsin B, and cytochrome c levels in ethanol group were significantly higher than control. Caspase-3, calpain levels were decreased in ethanol + betaine, ethanol + omega-3, and ethanol + omega-3 + betaine groups compared to ethanol group. Cathepsin B in ethanol + omega-3 + betaine group was decreased compared to ethanol, ethanol + betaine groups. Cathepsin L and DNA fragmentation were found not statistically significant. We found similar results in histological and morfometric parameters.

CONCLUSION

We found that pre- and postnatal ethanol exposure is capable of triggering necrotic cell death in rat brains, omega-3, and betaine reduce neurodegeneration. Omega-3 and betaine may prove beneficial for neurodegeneration, particularly in preventing FAS.

摘要

目的

我们旨在研究产前和产后乙醇暴露通过改良液体饮食对幼鼠大脑神经退行性变的影响,以阐明甜菜碱和ω-3补充剂的保护作用。当在产前和产后期间摄入乙醇时,可能会导致后代出现胎儿酒精综合征(FAS)。

方法

将大鼠分为对照组、乙醇组、乙醇+甜菜碱组、乙醇+ω-3组、乙醇+ω-3+甜菜碱组。通过生化分析细胞色素c、半胱天冬酶-3、钙蛋白酶、组织蛋白酶B和L、DNA片段化,以及组织学和形态计量学方法,评估甜菜碱和ω-3对乙醇诱导的大脑变化的反应效果。

结果

乙醇组中半胱天冬酶-3、钙蛋白酶、组织蛋白酶B和细胞色素c水平显著高于对照组。与乙醇组相比,乙醇+甜菜碱组、乙醇+ω-3组和乙醇+ω-3+甜菜碱组中半胱天冬酶-3、钙蛋白酶水平降低。与乙醇组、乙醇+甜菜碱组相比,乙醇+ω-3+甜菜碱组中组织蛋白酶B降低。组织蛋白酶L和DNA片段化无统计学意义。我们在组织学和形态计量学参数方面发现了类似结果。

结论

我们发现产前和产后乙醇暴露能够引发大鼠大脑中的坏死性细胞死亡,ω-3和甜菜碱可减少神经退行性变。ω-3和甜菜碱可能对神经退行性变有益,尤其是在预防胎儿酒精综合征方面。

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