AAS ›› 2014, Vol. 45 ›› Issue (5): 616-621.doi: 10.3969/j.issn.0529-1356.2014.05.006

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Ativation of gliacytes and p38 mitogen-activated protein kinase and possible mechanism of neuronal apoptosis induced by Aβ25-35 injection into hippocampus in rats

WANG Yuan-wei 1,2 ZHENG Guan-yi 1* CHEN Xiao-chun1 ZHANG Jing1 HUANG Tian-wen1 YE Hong1 PAN Xiao-dong1   

  1. 1. Department of Traditional Chinese Medicine,Fujian Medical University Union Hospital, Geriatric Research Institute of Fujian Province, Fuzhou 350001, China; 2. Department of Neurology, Shuyang People’s Hospital of Jiangsu Province, Jiangsu Shuyang 223600, China
  • Received:2013-12-09 Revised:2014-03-17 Online:2014-10-06 Published:2013-10-06
  • Contact: ZHENG Guan-yi E-mail:ycyz99@163.com

Abstract:

Objective To investigate the relationship between activation of gliacytes, mitogen-activated protein kinase (p38MAPK) and neuronal apoptosis after microinjecting aggregated Aβ25-35 into hippocampus. Methods The model was established by using stereotaxic technique to inject 10μg aggregated Aβ25-35 into dorsal hippocampus in rats. The rats were grouped as the control, vehicle and model groups. Immunohistochemistry and Western blotting were used for detection of activation of microglia(MG), atrocytes (AS) and expression of p-p38MAPK in the hippocampus. ELISA was used to evaluate the level of TNF-α and IL-1β. The survival neurons were observed by Nissl staining and the apoptotic neurons were identified by tunnel staining. Results Expression of ox-42, GFAP, p-p38MAPK were up-regulated in hippocampus, as well as TNF-α、IL-1β, which reached a highest value on the 7th day after injection of Aβ25-35. However, the number of neuron with Nissl positive decreased gradually, and the tunnel positive neurons increased highly and reached a peak value on the 7th day.There were significant differences between the control and vehicle group(P<0.01). Conclusion Apoptosis of the neuron caused by Aβ25-35 injection may result from activation of gliacytes, p38 MAPK and increase of TNF-α and IL-1β level.

Key words: Alzheimer’s disease, Amyloid protein β, P38 mitogen-activated protein kinases, Gliacyte, Hippocampal neuron,  , Wstern blotting, Rat