ω-3多不饱和脂肪酸通过CREB/BDNF/TrkB途径预防MK-801诱导的精神分裂症大鼠认知障碍。
ω-3PUFAs prevent MK-801-induced cognitive impairment in schizophrenic rats via the CREB/BDNF/TrkB pathway.
作者信息
Fang Mao-Sheng, Li Xing, Qian Hong, Zeng Kuan, Ye Meng, Zhou Yong-Jie, Li Hui, Wang Xiao-Chuan, Li Yi
机构信息
Wuhan Mental Health Center, Wuhan, 430022, China.
Department of Pathophysiology, School of Basic Medicine and the Collaborative Innovation Center for Brain Science, Key Laboratory of Ministry of Education of China for Neurological Disorders, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
出版信息
J Huazhong Univ Sci Technolog Med Sci. 2017 Aug;37(4):491-495. doi: 10.1007/s11596-017-1762-4. Epub 2017 Aug 8.
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.
本研究旨在确定ω-3多不饱和脂肪酸（ω-3PUFAs）对MK-801诱导的精神分裂症（SZ）大鼠认知障碍的保护作用及其潜在机制。采用MK-801诱导大鼠精神分裂症模型。利用Morris水迷宫评估大鼠的认知功能。通过尼氏染色测量海马神经元数量。采用蛋白质免疫印迹法检测大鼠海马中CREB、p-CREB、BDNF、TrkB、p-TrkB、AKT、p-AKT、ERK和p-ERK的表达。结果显示，ω-3PUFAs减轻了MK-801诱导的认知障碍和海马神经元丢失，逆转了MK-801诱导的CREB/BDNF/TrkB通路损伤，并拮抗了MK-801诱导的大鼠海马中p-AKT和p-ERK的下调。总之，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并减少神经元丢失，拮抗MK-801诱导的精神分裂症大鼠认知障碍。
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