Zhang Yan-Mei, Wu Wei, Ma Wei, Wang Fang, Yuan Jun
Department of Neurology, Inner Mongolia Autonomous Region People's Hospital, Hohhot, Inner Mongolia Autonomous Region, China.
Department of Brain Center, The Second Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang Province, China.
Neural Regen Res. 2017 Jul;12(7):1152-1158. doi: 10.4103/1673-5374.211196.
Glycosides of (GC) is a preparation used extensively for its neuroprotective effect against neurological diseases, but its mechanisms of action remains incompletely understood. Here, we established a bilateral common carotid artery occlusion model of vascular dementia in rats and injected the model rats with a suspension of GC (10 mg/kg/day, intraperitoneally) for 14 consecutive days. Immunohistochemistry showed that GC significantly reduced p-tau and amyloid beta (Aβ) immunoreactivity in the hippocampus of the model rats. Proteomic analysis demonstrated upregulation of mitochondrial precursor protein and downregulation of keratin type II cytoskeletal 6A after GC treatment compared with model rats that had received saline. Western blot assay confirmed these findings. Our results suggest that the neuroprotective effect of GC in vascular dementia occurs the promotion of neuronal cytoskeleton regeneration.
(原文中“Glycosides of (GC)”表述不完整,推测可能是某种物质的糖苷,这里按“(GC)糖苷”翻译)(GC)糖苷是一种因其对神经疾病的神经保护作用而被广泛使用的制剂,但其作用机制仍未完全明确。在此,我们建立了大鼠血管性痴呆双侧颈总动脉闭塞模型,并连续14天给模型大鼠腹腔注射(GC)糖苷混悬液(10毫克/千克/天)。免疫组织化学显示,(GC)糖苷显著降低了模型大鼠海马体中p - tau和β淀粉样蛋白(Aβ)的免疫反应性。蛋白质组学分析表明,与接受生理盐水的模型大鼠相比,(GC)糖苷处理后线粒体前体蛋白上调,II型角蛋白细胞骨架6A下调。蛋白质印迹分析证实了这些发现。我们的结果表明,(GC)糖苷在血管性痴呆中的神经保护作用是通过促进神经元细胞骨架再生实现的。