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

[ Vol. 29 , Issue. 30 ]


Xingjian Li, Qiyin Deng, Yaoyun Kuang, Hengxu Mao, Meiling Yao, Changsong Lin, Xiaodong Luo and Pingyi Xu*   Pages 2426 - 2437 ( 12 )


Background: The overexpression, accumulation, and cell-to-cell transmission of α-synuclein leads to the deterioration of Parkinson’s disease (PD). Previous studies suggest that Baicalein (BAI) can bind to α-synuclein and inhibit α-synuclein aggregation and secretion. However, it is still unclear whether BAI can intervene with the pathogenic molecules in α-synuclein-mediated PD pathways beyond directly targeting α-synuclein per se.

Methods: This study aimed to systematically investigate BAI’s potential targets in PD-related A53T mutant α-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 α-synucleinmediated pathways. NFKB1, STAT3, and CDKN1A are BAI’s potential hub targets in these pathways.

Conclusion: Our findings highlight BAI's potentiality to modulate α-synuclein-mediated pathways beyond directly targeting α-synuclein per se.


&#945;-synuclein, Baicalein, bioinformatics, Parkinson’s disease, neurodegenerative, pathological.


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