中国神经再生研究(英文版) ›› 2017, Vol. 12 ›› Issue (7): 1152-1158.doi: 10.4103/1673-5374.211196

• 原著:退行性病与再生 • 上一篇    下一篇

肉苁蓉总苷干预血管性痴呆大鼠线粒体前体蛋白和角蛋白II型细胞骨架6A的表达

  

  • 收稿日期:2017-06-19 出版日期:2017-07-15 发布日期:2017-07-15
  • 基金资助:

    中国国家自然科学基金项目(30960520),内蒙古自治区自然科学基金项目(2016MS0837

Effect of glycosides of Cistanche on the expression of mitochondrial precursor protein and keratin type II cytoskeletal 6A in a rat model of vascular dementia

Yan-mei Zhang1, Wei Wu2, Wei Ma3, Fang Wang4, Jun Yuan1   

  1. 1 Department of Neurology, Inner Mongolia Autonomous Region People’s Hospital, Hohhot, Inner Mongolia Autonomous Region, China; 2 Department of Brain Center, The Second Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang Province, China; 3 First Hospital of Wuhan, Wuhan, Hubei Province, China; 4 Jianghan University, Wuhan, Hubei Province, China
  • Received:2017-06-19 Online:2017-07-15 Published:2017-07-15
  • Contact: Jun Yuan, zhangyanmei2277@sina.com.
  • Supported by:

    This study was supported by the National Natural Science Foundation of China, No. 30960520; the Natural Science Foundation of Inner Mongolia Autonomous Region of China, No. 2016MS0837.

摘要:

研究显示肉苁蓉总苷对神经疾病中有神经保护作用,但遗憾的是其作用机制长期无专家共识。为此实验以双侧颈总动脉闭塞方法建立大鼠痴呆模型,然后连续14d腹腔注射100mg/kg/d肉苁蓉总苷混悬液,以免疫组化染色见肉苁蓉总苷能显著降低痴呆大鼠海马组织中磷酸化tau蛋白及Aβ的免疫阳性反应,以蛋白组学分析见海马组织中促进线粒体活性的伴侣蛋白——线粒体前体蛋白的表达增加,而与细胞结构有关的角蛋白II型细胞骨架6A表达下降,且Western blot分析也验证了此结果。说明肉苁蓉总苷可通过促进神经细胞骨架再生而对血管性痴呆有神经保护作用。

ORCID:0000-0002-0469-1203(Yan-mei Zhang)

关键词: 神经再生, 血管性痴呆, 肉苁蓉总苷, 线粒体前体蛋白, 角蛋白6A, 蛋白质组学, 神经保护

Abstract:

Glycosides of Cistanche (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 via the promotion of neuronal cytoskeleton regeneration.

Key words: nerve regeneration, vascular dementia, glycosides of Cistanche, mitochondrial precursor protein, keratin type II cytoskeletal 6A, proteomics, neuroprotection, neural regeneration