Cerebroprotein Hydrolysate-I Inhibits Hippocampal Neuronal Apoptosis by Activating PI3K/Akt Signaling Pathway in Vascular Dementia Mice

Introduction: Vascular dementia (VaD), one of the brain injuries, is difficult to be cured, so it is important to take active neuroprotective treatment after its occurrence. Many studies have shown that apoptosis serves an important role in VaD occurrence; therefore, inhibition of apoptosis may cont...

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Published inNeuropsychiatric disease and treatment Vol. 17; p. 2359
Main Authors Wu, Xiaolin, Liu, Yingjuan, Zhu, Lin, Wang, Yue, Ren, Yuqian, Cheng, Baohe, Ren, Leiming, Ge, Keli, Li, Hongyun
Format Journal Article
LanguageEnglish
Published Dove Medical Press Limited 31.07.2021
Subjects
Apoptosis
Binswanger's disease
Brain
Care and treatment
Cellular signal transduction
Development and progression
Health aspects
Hippocampus (Brain)
Injuries
Neuropeptides
Neuroprotective agents
Pharmacology, Experimental
Protein kinases
Vascular dementia
China
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Summary:Introduction: Vascular dementia (VaD), one of the brain injuries, is difficult to be cured, so it is important to take active neuroprotective treatment after its occurrence. Many studies have shown that apoptosis serves an important role in VaD occurrence; therefore, inhibition of apoptosis may contribute to the recovery of neurological function after VaD occurrence. Cerebroprotein hydrolysate-I (CH-I), a neuropeptide preparation which consists of several amino acids and small molecular peptides as the main active constituent, is extracted using a method similar to cerebrolysin (CBL) which has neuroprotective and neurotrophic effects. Methods: In the present study, a VaD model which was constructed using bilateral common carotid artery occlusion (BCCAO) in Kunming mice was applied to examine the neuroprotective effects of CH-I. Results: The results show that CH-I treatment could attenuate the decrease of learning and memory ability, cell apoptosis in the hippocampal CA1 region and inhibit the activation of caspase-3 and caspase-9 in VaD mice. Furthermore, CH-I treatment could also upregulate Bcl-2 protein levels and activate PI3K and Akt. Discussion: We speculate that CH-I may induce a neuroprotective effect activating PI3K/Akt signaling pathway in VaD mice. Keywords: vascular dementia, cerebroprotein hydrolysate-I, apoptosis, PI3K/Akt
ISSN:1176-6328
1178-2021
DOI:10.2l47/NDT.S311760