Protective effects of paeonol on human neuroblastoma cells in Parkinson's disease model and its underlying mechanism
10.11855/j.issn.0577-7402.0483.2024.0716
- VernacularTitle:丹皮酚对人神经母细胞瘤细胞帕金森病模型的保护作用及其初步机制
- Author:
Sheng-Nan SUN
1
;
Lu-Lu HE
;
Shao-Chen QIN
;
Lei XU
;
Li-Ran WANG
;
Bao-Feng YU
;
Cun-Gen MA
;
Hui-Jie FAN
;
Zhi CHAI
Author Information
1. 山西中医药大学多发性硬化益气活血重点研究室/神经生物学研究中心,山西 晋中 030619
- Keywords:
paeonol;
Parkinson's disease;
α-synuclein;
autophagy
- From:
Medical Journal of Chinese People's Liberation Army
2025;50(1):69-75
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the protective effects of paeonol(PAE)on autophagy in human neuroblastoma cells(SH-SY5Y)induced by overexpression of α-synuclein(α-Syn),and to explore its related mechanism.Methods SH-SY5Y cells served as control group,while those induced with A53T-α-Syn mutation were used as model group.Additional groups included PAE(150 μg/ml)group,3-MA(1 mmol/L)group,and PAE(150 μg/ml)+3-MA(1 mmol/L)group.Cell viability was assessed using CCK-8 method,cell morphology was observed under an optical microscope,and protein expressions of α-Syn,LC3-Ⅱ,p62,Beclin-1,phosphorylated c-Jun N-terminal kinase(p-JNK),and p-Bcl-2 were determined by Western blotting.Results Compared with control group,model control exhibited decreased cell survival(P＜0.01),increased α-Syn expression(P＜0.001),reduced expression of autophagy-related proteins LC3-Ⅱ and Beclin-1(P＜0.01,P＜0.05),elevated autophagy substrate protein p62(P＜0.05),and decreased expression of autophagy pathway-related proteins p-JNK and Bcl-2(P＜0.05,P＜0.01).Compared with model group,PAE group showed increased cell survival(P＜0.01),decreased α-Syn and p62 protein expression(P＜0.01,P＜0.05),and increased expression of LC3-Ⅱ,Beclin-1,p-JNK and Bcl-2(P＜0.05).Compared with PAE group,3-MA+PAE group demonstrated increased α-Syn expression(P＜0.05).Conclusions PAE could attenuate the injury of SH-SY5Y cells induced by A53T-α-Syn and eliminate over-expressed α-Syn by activating autophagy pathway,which may be associated with the upregulation of JNK/Bcl-2 mediated autophagy pathway.
