首页 | 本学科首页   官方微博 | 高级检索  
   检索      


Nerve Growth Factor is a Potential Treated Target in Tg(SOD1*G93A)1Gur Mice
Authors:Xu  Zhenzhen  Jiang  Jianxiang  Xu  Shengyuan  Xie  Zunchun  He  Pei  Jiang  Shishi  Xu  Renshi
Institution:1.Department of Neurology, Jiangxi Provincial People’s Hospital, Affiliated People’s Hospital of Nanchang University, Nanchang, 330006, Jiangxi, China
;2.Department of Neurology, First Affiliated Hospital of Nanchang University, Nanchang, 330006, Jiangxi, China
;
Abstract:

Nerve growth factor (NGF) is a protective factor of neural cells; the possible relationship between the NGF and the pathogenesis of amyotrophic lateral sclerosis (ALS) hasn’t been completely known. In this study, we observed and analyzed the expression and distribution of NGF, as well as the possible relationship between the NGF expression and distribution and the neural cell death in both SOD1 wild-type (WT) and Tg(SOD1*G93A)1Gur (TG) mice applying the fluorescence immunohistochemistry method. The results showed that the expression and distribution of NGF in the anterior horn (AH), the lateral horn (LH), and the surrounding central canal (CC) significantly increased at the supper early stage of ALS (Pre-onset stage) and the early stage (Onset stage), but the NGF expression and distribution in the AH, the LH, and the surrounding CC significantly reduced at the progression stage. The astrocyte, neuron, and oligodendrocyte produced the NGF and the neural precursor cells (NPCs) produced the NGF. The neural cell death gradually increased accompanying with the reduction of NGF expression and distribution. Our data suggested that the NGF was a protective factor of neural cells, because the neural cells in the AH, the LH, and the surrounding CC produced more NGF at the supper early and early stage of ALS; moreover, the NPCs produced the NGF. It implied that the NGF exerted the protective effect of neural cells, prevented from the neural cell death and aroused the potential of self-repair in the development of ALS.

Keywords:
本文献已被 SpringerLink 等数据库收录!
设为首页 | 免责声明 | 关于勤云 | 加入收藏

Copyright©北京勤云科技发展有限公司  京ICP备09084417号