Protective effect of Notch1-regulated microglial polarization against epileptic seizure in mice
10.12007/j.issn.0258-4646.2025.03.008
- VernacularTitle:Notch1蛋白调控的小胶质细胞极化对小鼠癫痫发作的保护作用
- Author:
Yangyang ZHU
1
;
Meng LIU
;
Daodi YANG
;
Yiyi HU
;
Jingxian FANG
Author Information
1. 南阳市第一人民医院神经内科,河南 南阳 473000
- Publication Type:Journal Article
- Keywords:
Notch1;
microglia;
polarization;
inflammatory reaction;
epilepsy
- From:
Journal of China Medical University
2025;54(3):228-232
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the protective effect of Notch1-regulated microglial polarization against epileptic seizure in mice.Methods The pentylenetetrazole(PTZ)kindling models of epilepsy were established in mice with normal(Notch1normal)and high(Notch1over)expression of the Notch1 protein,with Racine grade Ⅳ set as the standard,to evaluate the effect of Notch1 expression on sei-zure susceptibility.Microglial activation and polarization in the temporal lobe tissues of mice were detected using immunofluorescence staining,and the levels of inflammatory cytokines in the temporal lobe tissues was detected using an enzyme-linked immunosorbent assay.Results High Notch1 expression showed high resistance to seizures.Compared with the Notch1normal+Sal group,the relative fluorescence intensity of Iba1,CD16,and Arg1 proteins in the temporal lobes of mice in the Notch1normal+PTZ group,as well as the TNF-α,IL-6,and IL-10 levels significantly increased(P<0.05).Compared with the Notch1nornal+PTZ group,the relative fluorescence intensity of Iba1 and CD16 proteins in the temporal lobes of mice in the Notch1over+PTZ group significantly decreased(P<0.05),the relative fluorescence intensity of Arg1 protein significantly increased(P<0.05),the TNF-α and IL-6 levels significantly decreased(P<0.05),and the IL-10 level further increased(P<0.05).Conclusion High Notch1 protein expression significantly enhanced M2-type microglial polari-zation,inhibited M1-type microglial polarization,and increased resistance to seizure susceptibility in mice.