Study on the Molecular Mechanism of Baicalin Phosphorylation of Tau Protein Content in a Cell Model of Intervention Cognitive Impairment.

Objective: This study aimed to predict the molecular mechanism of baicalein through network pharmacology, cell experiments and molecular docking. The goal was to elucidate the mechanism for the treatment of mild cognitive impairment.

Materials And Methods: The protein-protein interaction network (PPI) and Cytoscape software were used to screen the hub genes of intersection genes, while the therapeutic mechanism of baicalein was predicted through the Gene ontology (GO) and Kyoto Encyclopedia of Gene and Genomes (KEGG) enrichment analysis. Molecular docking of the core target and baicalein was conducted using AutoDock software. The neuroprotective effect of Baicalein with different concentrations on okadaic acid-treated SH-SY5Y cells was investigated in cell experiments. Scratch experiments were conducted to explore the effect of baicalein on cell migration ability, and enzyme linked immunosorbent assay was employed to measure the content of extracellular pathological proteins. Western Blot and Cellular immunofluorescence pinpointed differences in the relevant protein content.

Results: Enrichment analysis revealed significant enrichment in the PI3K-Akt signaling pathway, and molecular docking demonstrated a favorable binding energy between baicalein and AKT1. In cell experiments, baicalein presented a positive impact on mild cognitive impairment by elevating P-AKT1 and P-GSK-3β levels while reducing the overall amount of P-tau.

Conclusion: As demonstrated by the present study, the low concentration of baicalein (15μmol/L) effectively managed the mild cognitive impairment by regulating the phosphorylation of AKT1 and GSK-3β.