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脑蛋白水解物-I 激活 PI3K/Akt 信号通路抑制血管性痴呆小鼠海马神经元凋亡
Authors Wu X, Liu Y, Zhu L, Wang Y, Ren Y, Cheng B, Ren L, Ge K, Li H
Received 1 April 2021
Accepted for publication 25 June 2021
Published 17 July 2021 Volume 2021:17 Pages 2359—2368
DOI https://doi.org/10.2147/NDT.S311760
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 2
Editor who approved publication: Dr Yuping Ning
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