Zhiqiang Lu,Jingqi Yang,Xiaomeng Xu,Ruowen Liu,Songyi Lin
Memory impairment affects cognition and information processing, and attention, leading to a decline in life quality of patients. Previous studies have shown the memory-improving effects of sea cucumber peptides. This study further explored the memory-improving mechanisms of sea cucumber peptides using scopolamine-induced memory-impaired mice and identified novel memory-improving peptides within low molecular weight peptide fractions. The sea cucumber peptides were categorized into three groups based on their molecular weights: SCP-L (molecular weight greater than 10 kDa), SCP-M (weight between 3 kDa and 10 kDa), and SCP-S (molecular weight less than 3 kDa). The results showed that SCP-S improved behavioral performance by regulating cholinergic system disorder and reducing oxidative stress levels, distinguishing itself from SCP-M and SCP-L. Further, SCP-S was found to exhibit a well ability in alleviating the degree of neuroinflammation dependent on microglia and promoting synaptic plasticity. Additionally, a novel memory-improving peptide Ser-Phe-Gly-Asp-Ile (SFGDI) was identified by EASY-nano-LC/MS/MS after simulated digestion-absorption coupling of in silico technologies from SCP-S. SFGDI protected against oxidative stress and regulated cholinergic system in scopolamine-induced PC12 cells. These findings suggest that SCP-S and SFGDI might be considered as potential memory-improving food for people suffering from memory disorders.
The peptide Ser-Phe-Gly-Asp-Ile (SFGDI), derived from sea cucumber, has demonstrated neuroprotective effects in cell models; however, the in vivo neuroprotective efficacy of SFGDI remains unexplored. In this study, we utilized a cognitive disorder mouse model induced by scopolamine and observed that daily oral administration of SFGDI at a dosage of 40 mg/kg resulted in improved behavioral performance in the Passive avoidance test, the Channel-type water maze test, and the Novel object recognition test (P < 0.05). Furthermore, our investigation into the underlying neuroprotective mechanisms of SFGDI revealed that it reduced oxidative stress levels through the activation of the Sirt3/SOD/ROS pathway, thereby balancing hippocampal unsaturated lipids (P < 0.05) in the mouse hippocampus. Moreover, SFGDI significantly decreased hippocampal neuroinflammation by modulating the activation of microglia and hypertrophy of astrocytes. Additionally, SFGDI was found to enhance synaptic plasticity in the mouse hippocampus by activating the ChAT/p-CaMKⅡ/BDNF pathway and increasing spine density in neuron cells (P < 0.05), particularly mushroom spines (P < 0.05). These experiments demonstrate that SFGDI exhibits neuroprotective effects by regulating hippocampal oxidative stress through the Sirt3/SOD/ROS pathway and synaptic plasticity via the ChAT/p-CaMKⅡ/BDNF pathway in the mouse hippocampus, thus emerging as a potential neuro-nutraceutical agent for alleviating memory impairment.
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