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

Abstract

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.

Analysis of Potential Mechanism of Herbal Formula Taohong Siwu Decoction against Vascular Dementia Based on Network Pharmacology and Molecular Docking

“…In this study, it was revealed that the therapeutic effects of TSD on VaD are mostly attributed to the potential core targets of AKT1, CASP3, IL1 β , JUN, and TP53, which are associated with cell apoptosis and inflammatory. Through Akt activation, the p-Akt protein was produced, which inhibited apoptosis and promoted hippocampal nerve cell survival [ 24 ]. The increased levels of cleaved caspase-3 protein and activation of the caspase-3 pathway promoted the apoptosis that occurred in the progression of chronic cerebral hypoperfusion to VaD [ 25 ].…”