Abstract
Schisandra chinensis (Turcz.) Baill (SC) is a traditional sedative in China, with wide applications for treating various neurological disorders. Its polysaccharide component has been gaining increased attention for its potential in nerve protection. While raw SC is the primary focus of current research, its processed products are primarily utilized as clinical medicines. Notably, limited research exists on the mechanisms underlying the effects of wine-processed Schisandra chinensis polysaccharide (WSCP) in Alzheimer's Disease (AD). Therefore, this study seeks to assess the therapeutic impact of WSCP on AD mice and investigate the underlying mechanisms through biochemical and metabolomics analyses. The results demonstrate that WSCP exerts significant therapeutic effects on AD mice by enhancing learning and memory abilities, mitigating hippocampal neuronal damage, reducing abnormal amyloid-beta (Aβ) deposition, and attenuating hyperphosphorylation of Tau. Biochemical analysis revealed that WSCP can increase SOD content and decrease MDA, IL-6, and TNF-α content in AD mice. Furthermore, serum metabolomic results showed that WSCP intervention can reverse metabolic disorders in AD mice. 43 endogenous metabolites were identified as potential biomarkers for WSCP treatment of AD, and the major metabolic pathways were Ala, Glu and Asp metabolism, TCA cycle. Overall, these findings will provide a basis for further development of WSCP.
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