Garlic-Derived Allicin Attenuates Parkinson’s Disease via PKA/p-CREB/BDNF/DAT Pathway Activation and Apoptotic Inhibition

Garlic-Derived Allicin Attenuates Parkinson’s Disease via PKA/p-CREB/BDNF/DAT Pathway Activation and Apoptotic Inhibition

Allicin (ALC), a naturally occurring organosulfur compound derived from garlic (<i>Allium sativum</i>), exhibits potential neuroprotective properties. Parkinson’s disease (PD) is a progressive neurodegenerative disease characterized by degeneration of dopaminergic neurons and motor dysfu...

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Bibliographic Details
Main Authors: Wanchen Zeng, Yingkai Wang, Yang Liu, Xiaomin Liu, Zhongquan Qi
Format: Article
Language:English
Published: MDPI AG 2025-08-01
Series:Molecules
Subjects:
allicin
Parkinson’s disease
network pharmacology
apoptosis
Online Access:https://www.mdpi.com/1420-3049/30/15/3265
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Summary:Allicin (ALC), a naturally occurring organosulfur compound derived from garlic (<i>Allium sativum</i>), exhibits potential neuroprotective properties. Parkinson’s disease (PD) is a progressive neurodegenerative disease characterized by degeneration of dopaminergic neurons and motor dysfunction. This study utilized bioinformatics and network pharmacology methods to predict the anti-PD mechanism of ALC and established in vivo and in vitro PD models using 6-hydroxydopamine (6-OHDA) for experimental verification. Network pharmacological analysis indicates that apoptosis regulation and the PKA/p-CREB/BDNF signaling pathway are closely related to the anti-PD effect of ALC, and protein kinase A (PKA) and dopamine transporter (DAT) are key molecular targets. The experimental results show that ALC administration can alleviate the cytotoxicity of SH-SY5Y induced by 6-OHDA and simultaneously improve the motor dysfunction and dopaminergic neuron loss in PD mice. In addition, ALC can also activate the PKA/p-CREB/BDNF signaling pathway and increase the DAT level in brain tissue, regulate the expression of BAX and Bcl-2, and reduce neuronal apoptosis. These results indicate that ALC can exert anti-PD effects by up-regulating the PKA/p-CREB/BDNF/DAT signaling pathway and inhibiting neuronal apoptosis, providing theoretical support for the application of ALC in PD.
ISSN:1420-3049

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