Analysis of Targeting Mechanism of Memory Enhancing Peptides Assisted by Antarctic Krill Based on the BCL-XL/Bax/Caspase-3/p53/CREB/BDNF Signaling Pathway
The study aimed to explore the preventive effect of Antarctic krill protein peptide(EHAK)on memory injury caused by scopolamine in mice.The mice were divided into 5 groups:Blank control group,memory damage model group,and low(31.25 mg/kg),medium(62.5 mg/kg)and high(125 mg/kg)dose groups of EHAK.The behavioral in-dices,serum and biochemical indices of the mice and the protein expression levels of hippocampal nerve cells were de-termined,and the states of hippocampal neurons were observed.Behavioral experiments indicated that EHAK could im-prove the spatial learning and memory ability of mice.Regarding the oxidative stress levels and cholinergic systems,when 125 mg/kg EHAK was administered to mice,compared with the model group,the SOD activity in serum increased by(10.13±1.00)U/mg prot and the MDA content in serum decreased by(1.04±0.26)nmol/mg prot.The hippocampal AChE activity and MDA content declined by(0.90±0.05)U/mg prot and(1.16±0.01)nmol/mg prot,respectively,while the ACh content increased by(10.13±1.00)μg/mg prot.These data indicated that EHAK could attenuate scopolamine-induced cognitive impairment by preventing oxidative stress and cholinergic dysfunction.The status of hippocampal neu-rons showed that the EHAK could effectively prevent hippocampal neuron apoptosis and uneven arrangement.In addition,EHAK could inhibit neuronal apoptosis and regulate prominent plasticity through the BCL-XUBax/Caspase-3/p53/CREB/BDNF signaling pathway.Therefore,EHAK could prevent scopolamine-induced memory impairment by modulating the cholinergic system and protecting neurons in the hippocampus,which demonstrated the potential to be used as food in-gredient with functional appeal.
Antarctic krill protein peptidememory impairmentsignaling pathway
万方数据
维普
