ω-3PUFAs prevent MK-801-induced cognitive impairment in schizophrenic rats via the CREB/BDNF/TrkB pathway.

Q Engineering Journal of Huazhong University of Science and Technology [Medical Sciences] Pub Date : 2017-08-01 Epub Date: 2017-08-08 DOI:10.1007/s11596-017-1762-4

Mao-Sheng Fang, Xing Li, Hong Qian, Kuan Zeng, Meng Ye, Yong-Jie Zhou, Hui Li, Xiao-Chuan Wang, Yi Li

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引用次数: 19

Abstract

This study was to determine the protective effect of ω-3 polyunsaturated fatty acids (ω-3PUFAs) on MK-801-induced cognitive impairment in schizophrenia (SZ) rats and the underlying mechanism. A rat model of schizophrenia was induced by MK-801. The cognitive function of rats was assessed using a Morris water maze. The number of hippocampal neurons was measured by Nissl staining. The expression of CREB, p-CREB, BDNF, TrkB, p-TrkB, AKT, p-AKT, ERK, and p-ERK in the hippocampus of rats was detected by Western blotting. The results showed that ω-3PUFAs attenuated MK-801-induced cognitive impairment and hippocampal neurons loss, reversed the injury of the CREB/BDNF/TrkB pathway induced by MK-801, and antagonized MK-801-induced down-regulation of p-AKT and p-ERK in the hippocampus of rats. In conclusion, ω-3PUFAs enhances the CREB/BDNF/TrkB pathway by activating ERK and AKT, thereby increasing the synaptic plasticity and decreasing neuron loss, and antagonizing MK-801-induced cognitive impairment in schizophrenic rats.

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ω-3PUFAs通过CREB/BDNF/TrkB途径预防mk -801诱导的精神分裂症大鼠认知障碍。

本研究旨在探讨ω-3多不饱和脂肪酸(ω-3PUFAs)对mk -801诱导的精神分裂症(SZ)大鼠认知功能障碍的保护作用及其机制。用MK-801诱导大鼠精神分裂症模型。采用Morris水迷宫法评估大鼠认知功能。采用尼氏染色法测定海马神经元数量。Western blotting检测大鼠海马组织中CREB、p-CREB、BDNF、TrkB、p-TrkB、AKT、p-AKT、ERK、p-ERK的表达。结果表明，ω-3PUFAs可减轻MK-801诱导的大鼠认知功能障碍和海马神经元丢失，逆转MK-801诱导的CREB/BDNF/TrkB通路损伤，拮抗MK-801诱导的海马p-AKT和p-ERK下调。综上所述，ω-3PUFAs通过激活ERK和AKT增强CREB/BDNF/TrkB通路，从而增加突触可塑性，减少神经元损失，拮抗mk -801诱导的精神分裂症大鼠认知功能障碍。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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