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在大脑中动脉闭塞动物模型和谷氨酸处理的HT22细胞中,缺血性脑损伤会降低发动蛋白样蛋白1的表达。

Ischemic brain injury decreases dynamin-like protein 1 expression in a middle cerebral artery occlusion animal model and glutamate-exposed HT22 cells.

作者信息

Jang Ah-Ram, Koh Phil-Ok

机构信息

Department of Anatomy, College of Veterinary Medicine, Research Institute of Life Science, Gyeongsang National University, Jinju, Korea.

出版信息

Lab Anim Res. 2016 Dec;32(4):194-199. doi: 10.5625/lar.2016.32.4.194. Epub 2016 Dec 23.

Abstract

Dynamin-like protein I (DLP-1) is an important mitochondrial fission and fusion protein that is associated with apoptotic cell death in neurodegenerative diseases. In this study, we investigated DLP-1 expression in a focal cerebral ischemia animal model and glutamate-exposed hippocampal-derived cell line. Middle cerebral artery occlusion (MCAO) was surgically induced in adult male rats to induce focal cerebral ischemic injury. Brain tissues were collected 24 hours after the onset of MCAO. MCAO induces an increase in infarct volume and histopathological changes in the cerebral cortex. We identified a decrease in DLP-1 in the cerebral cortices of MCAO-injured animals using a proteomic approach and Western blot analysis. Moreover, glutamate treatment significantly decreased DLP-1 expression in a hippocampal-derived cell line. The decrease in DLP-1 indicates mitochondrial dysfunction. Thus, these results suggest that neuronal cell injury induces a decrease in DLP-1 levels and consequently leads to neuronal cell death.

摘要

动力蛋白样蛋白1(DLP-1)是一种重要的线粒体分裂和融合蛋白,与神经退行性疾病中的凋亡细胞死亡有关。在本研究中,我们调查了局灶性脑缺血动物模型和谷氨酸暴露的海马来源细胞系中DLP-1的表达。通过手术诱导成年雄性大鼠大脑中动脉闭塞(MCAO)以诱导局灶性脑缺血损伤。在MCAO发作后24小时收集脑组织。MCAO导致梗死体积增加和大脑皮质的组织病理学变化。我们使用蛋白质组学方法和蛋白质印迹分析确定了MCAO损伤动物大脑皮质中DLP-1的减少。此外,谷氨酸处理显著降低了海马来源细胞系中DLP-1的表达。DLP-1的减少表明线粒体功能障碍。因此,这些结果表明神经元细胞损伤导致DLP-1水平降低,进而导致神经元细胞死亡。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2891/5206225/0688ede5f448/lar-32-194-g001.jpg

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