Scope: Cerebrosides are a class of neutral glycosphingolipids, which are widely found to be present in brain tissue. In this study, the protective effect of sea cucumber cerebrosides (Cer) against β-amyloid (Aβ)-induced cognitive impairment is investigated.
Methods and results: Male SD rats receive a ventricle injection Aβ1-42 peptide to establish an Alzheimer's disease model. Then, the protective effects of Cer against Aβ1-42 -induced cognitive impairment by gavage and feed addition are evaluated. The Morris water maze test results show that oral administration of Cer can significantly ameliorate Aβ1-42 -induced cognitive deficiency at both high dose (200 mg per kg·per day) and low dose (40 mg per kg·per day) for 27 days. Dietary supplement of Cer by feed addition also exhibits the amelioration on the impaired cognitive function. Further findings indicate that Cer ameliorates Aβ1-42 -induced neuronal damage and suppresses the induced apoptosis by decreasing the level of Bax/Bcl-2. Additionally, Cer enhances the expressions of PSD-95 and synaptophysin by activating BDNF/TrkB/CREB signaling pathway, thereby ameliorating Aβ1-42 -induced synaptic dysfunction. Furthermore, Cer attenuates Aβ1-42 -induced tau hyperphosphorylation by activating the PI3K/Akt/GSK3β signaling pathway.
Conclusion: Sea cucumber cerebrosides possess neuroprotective effects against Aβ1-42 -triggered cognitive deficits, which may be a potential nutritional preventive strategy for neurodegenerative diseases.
Keywords: Alzheimer's disease; cognitive deficiency; neuroprotection; sea cucumber cerebrosides; β-amyloid deposition.
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