Abstract

Baicalin has been shown to promote spatial learning and neural regeneration, which might increase the differentiation of neural stem cells in Alzheimer’s disease (AD) rat models. We aimed to study the role of baicalin on neuronal pentraxin-1 (NPTX-1), neuronal pentraxin-2 (NPTX-2), and C-reactive protein (CRP) in AD model rats.

The 30 male Sprague Dawley rats were divided into three groups: the control group, the AD model group, and the AD + baicalin group. Then, the Morris water maze was used to verify the effect of baicalin on the memory and spatial learning of rats. Immunohistochemistry and immunofluorescence were used to observe the expression of NPTX-1, NPTX-2, and CRP in brain tissue.

Compared with the AD model group, the AD rats treated with baicalin spent significantly less time finding escape latencies (P = 0.008) and had longer cross-platform times in the target quadrant (P = 0.015). In addition, the AD + baicalin group had significantly higher numbers of hippocampal neurons compared with the AD model group (P < 0.05). Baicalin also obviously decreased the apoptosis of neurons. Moreover, compared with the AD model group, the NPTX-1 and CRP expression in the AD + baicalin group was significantly reduced (P = 0.000) while the expression of NPTX-2 in the brain tissue of AD rats was significantly increased (P = 0.000).

Baicalin can play a therapeutic role by downregulating NPTX-1, upregulating NPTX-2, and downregulating CPR in AD model rats.

Details

Title
An interventional study of baicalin on neuronal pentraxin-1, neuronal pentraxin-2, and C-reactive protein in Alzheimer’s disease rat model
Author
Jing-Kun Zhao 1 ; Si-Jia Hou 2 ; Ji-Wei, Zhao 1 ; Hong-Li, Yu 1 ; Shu-Rong Duan 1   VIAFID ORCID Logo 

1  Department of Neurology, The First Affiliated Hospital of Harbin Medical University, No. 23 Postal Street, Nangang District, Harbin 150001, China 
2  Department of Neurology, The General Hospital of Heilongjiang Province Land Reclamation Bureau, Harbin 150088, China 
Publication year
2023
Publication date
2023
Publisher
De Gruyter Poland
ISSN
20813856
e-ISSN
20816936
Source type
Scholarly Journal
Language of publication
English
DOI
https://doi.org/10.1515/tnsci-2022-0298
ProQuest document ID
2861469536
Copyright
© 2023. This work is published under http://creativecommons.org/licenses/by/4.0 (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.