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首页> 外文期刊>Brain research >Involvement of decreased neuroglobin protein level in cognitive dysfunction induced by 1-bromopropane in rats
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Involvement of decreased neuroglobin protein level in cognitive dysfunction induced by 1-bromopropane in rats

机译：神经球蛋白水平下降与1-溴丙烷诱发的大鼠认知功能障碍的关系

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摘要

1-Bromopropane (1-BP) is used as a substitute for ozone-depleting solvents (ODS) in industrial applications. 1-BP could display central nervous system (CNS) neurotoxicity manifested by cognitive dysfunction. Neuroglobin (Ngb) is an endogenous neuroprotectant and is predominantly expressed in the nervous system. The present study aimed to investigate Ngb involvement in CNS neurotoxicity induced by 1-BP in rats. Male Wistar rats were randomly divided into 5 groups (n=14) and treated with 0, 100, 200, 400 and 800 mg/kg bw 1-BP, respectively, by gavage for consecutive 12 days. Rats displayed cognitive dysfunction dose-dependently through Morris water maze (MWM) test. Significant neuron loss in layer 5 of the prelimbic cortex (PL) was observed. Moreover, 1-BP decreased Ngb protein level in cerebral cortex and Ngb decrease was significantly positively correlated with cognitive dysfunction. Glutathione (GSH) content, GSH/oxidized glutathione (GSSG) ratio and glutamate cysteine ligase (GCL) activity decreased in cerebral cortex, coupled with the increase in GSSG content. GSH and GSH/GSSG ratio decrease were significantly positively correlated with cortical Ngb decrease. Additionally, levels of N-epsilon-hexanoyl-lysine (HEL) and 4-hydroxy-2-nonenal (4-HNE) modified proteins in cerebral cortex of 1-BP-treated rats increased significantly. In conclusion, it was suggested that 1-BP resulted in decreased endogenous neuroprotectant Ngb in cerebral cortex, which might play an important role in CNS neurotoxicity induced by 1-BP and that 1-BP-induced oxidative stress in cerebral cortex might partly be responsible for Ngb decrease. (C) 2014 Elsevier B.V. All rights reserved.
机译：1-溴丙烷（1-BP）在工业应用中替代臭氧消耗溶剂（ODS）。 1-BP可能显示以认知功能障碍为特征的中枢神经系统（CNS）神经毒性。神经球蛋白（Ngb）是一种内源性神经保护剂，主要在神经系统中表达。本研究旨在调查Ngb参与1-BP诱导的大鼠中枢神经系统神经毒性。将雄性Wistar大鼠随机分为5组（n ＝ 14），并分别通过管饲法分别给予0、100、200、400和800mg / kg bw 1-BP处理，连续12天。通过莫里斯水迷宫（MWM）测试，大鼠表现出剂量依赖性的认知功能障碍。在前肢皮层（PL）的第5层中观察到明显的神经元丢失。此外，1-BP降低大脑皮质Ngb蛋白水平，Ngb降低与认知功能障碍显着正相关。大脑皮层中谷胱甘肽（GSH）含量，谷胱甘肽/氧化型谷胱甘肽（GSSG）比率和谷氨酸半胱氨酸连接酶（GCL）活性降低，同时GSSG含量增加。 GSH和GSH / GSSG比值降低与皮质Ngb降低呈显着正相关。此外，在接受1-BP治疗的大鼠大脑皮层中，N-ε-己酸-赖氨酸（HEL）和4-羟基-2-壬烯（4-HNE）修饰蛋白的水平显着增加。结论提示1-BP降低了大脑皮层的内源性神经保护剂Ngb，这可能在1-BP诱导的中枢神经系统神经毒性中起重要作用，并且1-BP诱导的大脑皮层的氧化应激可能部分负责Ngb减少。 （C）2014 Elsevier B.V.保留所有权利。

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