Lithium chloride reduced the level of oxidative stress in brains and serums of APP/PS1 double transgenic mice via the regulation of GSK3ß/Nrf2/HO-1 pathway.
Int J Neurosci
; 130(6): 564-573, 2020 Jun.
Article
em En
| MEDLINE
| ID: mdl-31679397
ABSTRACT
Aim:
The aim of this study is to investigate whether lithium chloride (LiCl) can regulate glycogen synthase kinase-3ß (GSK3ß)/nuclear factor E2 related factorï¼Nrf2ï¼/heme oxygenase-1 (HO-1) pathway to reduce the injury of oxidative stress in APP/PS1 double transgenic mice.Materials andMethods:
The APP/PS1 double transgenic and wild-type (WT) mice were divided randomly into four groups, i.e. WT, WT + LiCl (LiCl 100 mg/kg by gavage once daily), the transgenic + LiCl and the transgenic groups. The expressions of phosphor-GSK3ß (ser9), Nrf2 and HO-1 at protein levels were detected by Western blotting. The activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), and the content of malondialdehyde (MDA) were measured by related detection kits. Nissl bodies in different brain regions were examined by Nissl staining.Results:
The decreased protein levels of phosphor-GSK3ß (ser9), Nrf2 and HO-1, the declined activities of SOD and GSH-Px, the increased content of MDA and the decreased Nissl bodies in neurons were observed in the brains or serums of APP/PS1 mice as compared with WT. The treatment with LiCl attenuated these changes in the levels of GSK3ß/Nrf2/HO-1 pathway and oxidative stress as well as Nissl bodies induced by APP/PS1 mutation.Conclusion:
LiCl reversed the declined activities of SOD and GSH-Px and the increased content of MDA as well as the decreased Nissl bodies in neurons in the brains or serums of APP/PS1 mice, the mechanism of which may be involved in the down-regulation of the activity of GSK3ß and consequently enhances the expressions of Nrf2 and HO-1.Palavras-chave
Texto completo:
1
Base de dados:
MEDLINE
Assunto principal:
Encéfalo
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Cloreto de Lítio
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Estresse Oxidativo
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Heme Oxigenase-1
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Fator 2 Relacionado a NF-E2
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Doença de Alzheimer
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Glicogênio Sintase Quinase 3 beta
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Proteínas de Membrana
Tipo de estudo:
Prognostic_studies
Limite:
Animals
Idioma:
En
Ano de publicação:
2020
Tipo de documento:
Article