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丁基苯酞通过PRDM5改善氧化应激引起的神经元细胞凋亡

何康 高永涛 徐晨阳 段国庆

中国临床药理学杂志2024,Vol.40Issue(1):17-21,5.
中国临床药理学杂志2024,Vol.40Issue(1):17-21,5.DOI:10.13699/j.cnki.1001-6821.2024.01.004

丁基苯酞通过PRDM5改善氧化应激引起的神经元细胞凋亡

3-butylphthalideimproves neuronal apoptosis induced by oxidative stress through PRDM5

何康 1高永涛 1徐晨阳 1段国庆1

作者信息

  • 1. 河南大学淮河医院神经外科,河南开封 475000
  • 折叠

摘要

Abstract

Objective To investigate the effects of 3-Butylphthalideon oxidative stress-induced apoptosis of neuronal cells PC-12 and its mechanism.Methods PC-12 cells were divided into four groups,Vector group:DMSO treated and transfected with vector plasmid;3-butylphthalide+vector group:DMSO+25 μmol·L-1 3-butylphthalidewas treated with vector plasmid was transfected;PRDM5 group:PR domain zinc finger protein 5(PRDM5)overexpression plasmid was transfected with DMSO;3-butylphthalide+PRDM5 group:Treated with DMSO+25 μmol·L-1 3-butylphthalide and transfected with PRDM5 overexpression plasmid.Apoptosis levels of neurons were detected by flow cytometry;Cleaved cysteine aspartate proteinase 3(Cleaved-caspase 3),B cell lymphoma-2(Bcl-2)and Bcl-2 associated X(Bax)expression levels were detected by Western blotting;binding sites of 3-Butylphthalideand PRDM5 were analyzed by molecular docking.Results The apoptosis levels of vector group,3-butylphthalide+vector group,PRDM5 group and 3-butylphthalide+PRDM5 group were(63.52±5.72)%,(20.48±3.56)%,(79.48±8.13)%and(22.58±3.01)%;Cleaved-caspase 3 expression levels were 0.89±0.09,0.29±0.03,1.12±0.09 and 0.31±0.05;the expression levels of Bcl-2 were 0.31±0.02,0.79±0.05,0.12±0.01 and 0.89±0.11;the expression levels of Bax were 0.83±0.08,0.25±0.03,1.03±0.11 and 0.27±0.03,respectively.The above indexes of Vector group were significantly different from those of PRDM5 group(all P<0.05).That 3-Butylphthalidewas bound to PRDM5(free energy-12.55 kcal·mol-1),and binding sites were K413R and D414A.Conclusion 3-butylphthalidebinds to K413R and D414A of PRDM5,inhibiting the function of PRDM5 and improving the apoptosis of neuronal cells induced by oxidative stress.

关键词

丁基苯酞/PR结构域蛋白5/氧化应激/神经元细胞/凋亡

Key words

3-butylphthalide/PR domain zinc finger protein 5/oxidative stress/neuron cell/apoptosis

分类

医药卫生

引用本文复制引用

何康,高永涛,徐晨阳,段国庆..丁基苯酞通过PRDM5改善氧化应激引起的神经元细胞凋亡[J].中国临床药理学杂志,2024,40(1):17-21,5.

基金项目

河南省科技厅攻关计划基金资助项目(232102310356) (232102310356)

中国临床药理学杂志

OA北大核心CSTPCD

1001-6821

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