期刊
NEUROSCIENCE LETTERS
卷 651, 期 -, 页码 72-78出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/j.neulet.2017.04.022
关键词
Vascular dementia; Cerebrolysin; BCCAO; Plasticity-related proteins; Apoptosis-related proteins
资金
- Hebei Province Major Medical Research Project of China [zd2013005]
- Hebei Province Natural Science Foundation of China [H2013307046]
The incidence of vascular dementia (VaD) has rapidly increased over the past few decades. Although officially approved medications for VaD remain limited, cerebrolysin (CBL) had preventive and treatment effects on VaD in some clinical trials. However, the underlying mechanisms have not been determined. The aim of this study was to determine whether CBL protects against cognitive deficits in a rat model of VaD induced by chronic cerebral hypoperfusion by increasing the levels of plasticity-related proteins and decreasing the levels of apoptosis-related proteins. In our study, adult male Sprague-Dawley rats were subjected to bilateral common carotid artery occlusion (BCCAO) surgery. The animals were randomly divided into four groups after the operation: Sham, Vehicle, L-CBL (2.5 ml/kg), and H-CBL (5 ml/kg). CBL was administered after the operation daily for 28 days. The CBL treatment significantly decreased the escape latency and increased the percentage of time the rat spent in the target quadrant of the Morris water maze (MWM) task. Pathological changes in the hippocampus, such as reduced cell count numbers and obvious pyknosis, were observed using haematoxylin-eosin (HE) staining. Furthermore, CBL significantly increased the expression of plasticity-related synaptic proteins, such as postsynaptic density protein 95 (PSD-95), protein kinase C subunit gamma (PKey), phosphorylated cAMP response element binding protein (p-CREB), and decreased the expression of apoptosis-related proteins in the hippocampus. In summary, CBL likely protects against cognitive deficits by improving synaptic plasticity and decreasing apoptosis. (C) 2017 Elsevier B.V. All rights reserved.
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