Ativation of gliacytes and p38 mitogen-activated protein kinase and possible mechanism of neuronal apoptosis induced by Aβ25-35 injection into hippocampus in rats
10.3969/j.issn.0529-1356.2014.05.006
- VernacularTitle:海马背侧注射β-淀粉样蛋白25~35激活胶质细胞和 p38丝裂原活化蛋白激酶诱导神经元凋亡
- Author:
Yuanwei WANG
;
Guanyi ZHENG
;
Xiaochun CHEN
;
Jing ZHANG
;
Tianwen HUANG
;
Hong YE
;
Xiaodong PAN
- Publication Type:Journal Article
- Keywords:
Alzheimer ’ s disease;
Amyloid protein β;
P38 mitogen-activated protein kinases;
Gliacyte;
Hippocampal neuron;
Wstern blotting;
Rat
- From:
Acta Anatomica Sinica
2014;(5):616-621
- CountryChina
- Language:Chinese
-
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-αand 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-αand IL-1βlevel.