Abstract
As is well documented, Alzheimer's disease (AD) is the most prevalent neurodegenerative disease. Meanwhile, Schisandra polysaccharide (SCP) has been reported to exert a protective effect on the nervous system and can regulate metabolic disorders in AD-like symptoms of amyloid β-peptide (Aβ) 25-35-induced rats. Nevertheless, the underlying mechanisms and metabolic markers for the diagnosis of AD are yet to be determined. This study aimed to explore the neuroprotective effect and potential mechanism of action of SCP in AD-like symptoms of Aβ25-35-induced rats by combining pharmacodynamics, metabolomics, and lipidomics. The pharmacodynamic results revealed that SCP significantly improved the spatial learning and long-term memory function and the morphology of neurons in the hippocampal CA1 region, alleviated inflammatory damage and oxidative stress, inhibited the activation of microglia and astrocytes, and increased the proportion of mature neurons of AD-like symptoms of Aβ25-35-induced rats. The results of hippocampal metabolomics and serum lipidomics showed 46 and 48 potential biomarkers were identified for the SCP treatment of AD, respectively. The involved pathways principally comprised lipid metabolism, amino acid metabolism, and energy metabolism. This study elucidates the neuroprotective effect of SCP in AD and its mechanism from the perspective of metabolomics and lipidomics and provides a theoretical basis for the therapeutic effect of SCP in AD.
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