The hippocampal proteomics mechanism of thalidomide in Alzheimer's disease model mice induced by Aβ
- Author:
Su-Hui WU
1
;
Han ZHANG
1
;
Yu-Hang ZHANG
1
;
Ting-Yuan NIU
1
;
Han-Bing LI
1
;
Jian-Feng GAO
1
;
Gen-Lin LI
1
Author Information
- Publication Type:Journal Article
- Keywords: Alzheimer's disease; biological information analysis; differential protein; hippocampus; mitochondria; proteomics
- From: Chinese Pharmacological Bulletin 2023;39(2):315-325
- CountryChina
- Language:Chinese
- Abstract: Aim To observe the effect of thalidomide on the learning and memory ability and hippocampal tissue proteome of Alzheimer's disease(AD)mice,to screen the differential proteins of thalidomide in preventing and treating AD,the pathways involved in regulation,and to explore its possible mechanism. Methods The experimental mice were randomly divided into blank control group,model group,and thalidomide high and low dose groups. The drugs were administered by gavage every day for 21 days. After the administration,Morris water maze test was used to evaluate the learning and memory abilities of the mice,HE staining and Nissl staining were used to observe the pathological tissue morphology of the mouse hippocampus,ELISA was employed to detect the mitochondrial respiratory chain enzyme complex in mouse brain,and the Label-free proteomics method was used to screen different groups of hippocampal proteome proteins. Results The results of the Morris water maze showed that compared with the model group,the escape latency time of the drug group was significantly reduced,and the number of crossing the platform significantly increased(P<0.05). Thalidomide administration could improve the morphological structure of neurons in hippocampus,and could increase the activity of the mitochondrial respiratory chain complex ,Ⅱ, and of the brain tissues of AD mice(P<0.05). A total of 4 378 differential proteins were identified,which had a significant regulatory effect on the expression of 580 proteins in hippocampus of AD mice(P<0.05). Energy metabolism may jointly participate in the regulation of neurodegeneration pathways-changes in pathways such as various diseases and Alzheimer's disease. Conclusions Thalidomide can significantly improve the learning and memory function of AD model mice induced by Aβ
