Identifying NFKB1, STAT3, and CDKN1A as Baicalein's Potential Hub Targets in Parkinson's Disease-related α-synuclein-mediated Pathways by Integrated Bioinformatics Strategies

摘要

Background: The overexpression, accumulation, and cell-to-cell transmission of alpha-synuclein leads to the deterioration of Parkinson's disease (PD). Previous studies suggest that Baicalein (BAI) can bind to alpha-synuclein and inhibit alpha-synuclein aggregation and secretion. However, it is still unclear whether BAI can intervene with the pathogenic molecules in alpha-synuclein-mediated PD pathways beyond directly targeting alpha-synuclein per se.Methods: This study aimed to systematically investigate BAI's potential targets in PD-related A53T mutant alpha-synuclein-mediated pathways by integrating data mining, network pharmacological analysis, and molecular docking simulation techniques.Results: The results suggest that BAI may target genes that are dysregulated in synaptic transmission, vesicle trafficking, gene transcription, protein binding, extracellular matrix formation, and kinase activity in alpha-synuclein-mediated pathways. NFKB1, STAT3, and CDKN1A are BAI's potential hub targets in these pathways.Conclusion: Our findings highlight BAI's potentiality to modulate alpha-synuclein-mediated pathways beyond directly targeting alpha-synuclein per se.

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