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

Author(s):

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

Abstract:

<p>Background: The overexpression, accumulation, and cell-to-cell transmission of &#945;-synuclein leads to the deterioration of Parkinson’s disease (PD). Previous studies suggest that Baicalein (BAI) can bind to &#945;-synuclein and inhibit &#945;-synuclein aggregation and secretion. However, it is still unclear whether BAI can intervene with the pathogenic molecules in &#945;-synuclein-mediated PD pathways beyond directly targeting &#945;-synuclein per se. </p><p> Methods: This study aimed to systematically investigate BAI’s potential targets in PD-related A53T mutant &#945;-synuclein-mediated pathways by integrating data mining, network pharmacological analysis, and molecular docking simulation techniques. </p><p> 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 &#945;-synucleinmediated pathways. <i>NFKB1, STAT3</i>, and <i>CDKN1A</i> are BAI’s potential hub targets in these pathways. </p><p> Conclusion: Our findings highlight BAI's potentiality to modulate α-synuclein-mediated pathways beyond directly targeting α-synuclein per se.</p>

Keywords:

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

Affiliation:

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