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Current Pharmaceutical Design

Editor-in-Chief

ISSN (Print): 1381-6128
ISSN (Online): 1873-4286

Research Article

Identifying NFKB1, STAT3, and CDKN1A 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*

Volume 29, Issue 30, 2023

Published on: 18 October, 2023

Page: [2426 - 2437] Pages: 12

DOI: 10.2174/0113816128259065231011114116

Price: $65

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Abstract

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.

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