Effects of cattle encephalon glycoside and ignotin on the expression of glial fibrillary acidic protein and neuronal nuclear antigen in the brain of the APP/PS1 mouse models of Alzheimer's disease
10.3760/cma.j.issn.0254-9026.2020.09.018
- VernacularTitle:脑苷肌肽对APP/PS1阿尔茨海默病模型小鼠脑内胶质纤维酸性蛋白和神经元核抗原表达的影响
- Author:
Yinghan ZHANG
1
;
Yazhuo HU
;
Zhitao HAN
;
Ya GAO
;
Ruisheng LI
;
Eryan KONG
;
Xiaoning WANG
;
Zhongjian ZHANG
;
Honghong ZHANG
Author Information
1. 新乡医学院精神神经医学研究院 453003
- From:
Chinese Journal of Geriatrics
2020;39(9):1067-1071
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To investigate the effects of cattle encephalon glycoside and ignotin(CEGI)on the expression of glial fibrillary acidic protein(GFAP)and neuronal nuclear antigen(NeuN)in the brain of APP/PS1 model mice of Alzheimer's disease.Methods:A total of 36 5-month-old APP/PS1 dual-transgenic model mice were randomly divided into 3 groups: the model group(normal saline 6.6 ml·kg -1·d -1), CEGI group(CEGI 6.6 ml·kg -1·d -1)and donepezil group(donepezil 2 mg·kg -1·d -1), with 12 in each group.Twelve C57BL/6J mice of the same age were used as the normal control group.All mice were given drugs for 6 weeks consecutively.Brain tissue was collected for immunohistochemical staining to detect the expression of amyloid β-protein(Aβ), GFAP and NeuN, which were then analyzed quantitatively. Results:The results of immunohistochemical staining indicated that levels of Aβ and GFAP were higher and levels of NeuN were lower in the model group than in the normal control group(0.147±0.068% vs.0%, 61.750±22.020 vs.26.000±4.598, 0.021±0.002 vs.0.032±0.003, P<0.05). Levels of Aβ and GFAP were lower and levels of NeuN were higher in the CEGI group and the donepezil group than in the model group(0.058±0.055 % vs.0.057±0.045 %, 38.250±5.418 vs.36.130±5.963, 0.029±0.004 vs.0.027±0.003, P<0.05). There was no significant difference in the expression of Aβ, GFAP and NeuN between the CEGI group and the donepezil group( P>0.05). Conclusions:CEGI has multi-target neuroprotective effects via down-regulating the expression of Aβ and GFAP and up-regulating the expression of NeuN.
