Glycyrrhizin regulates the HMGB1/P38MAPK signalling pathway in status epilepticus.
Mol Med Rep
; 27(2)2023 Feb.
Article
em En
| MEDLINE
| ID: mdl-36633134
ABSTRACT
In recent decades, studies have reported that inflammation serves key roles in epilepsy and that high mobility group box protein1 (HMGB1) may be involved in status epilepticus. However, it has not been reported whether HMGB1 participates in the pathogenesis of status epilepticus through the regulation of the p38 mitogenactivated protein kinase (p38MAPK) signalling pathway. In the present study, SpragueDawley rats were randomly divided into four groups as follows Control, status epilepticus (SE), dimethyl sulfoxide treatment (DMSO + SE), and glycyrrhizin treatment (GL + SE) groups. Behavioural changes were then evaluated using the Racine score. In the hippocampus, the protein expression levels of HMGB1 were assessed using western blotting, the neuronal damage was evaluated using haematoxylin and eosin staining and transmission electron microscopy, and the activation of microglia was assessed using immunochemistry and immunofluorescence. The results demonstrated that, in the hippocampal region, HMGB1 existed in neurons and astrocytes and the protein expression levels of HMGB1, p38MAPK and phosphorylatedp38MAPK were significantly inhibited after treatment with GL. Furthermore, GL could alleviate neuronal injury in the CA1 region of the hippocampus and prevented HMGB1 translocation from the nucleus into the cytoplasm in these areas. These findings expand the understanding of how HMGB1 may participate in SE and lay a foundation for evaluation of HMGB1 as a drug target.
Palavras-chave
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Estado Epiléptico
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Ácido Glicirrízico
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Proteína HMGB1
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Proteínas Quinases p38 Ativadas por Mitógeno
Limite:
Animals
Idioma:
En
Revista:
Mol Med Rep
Ano de publicação:
2023
Tipo de documento:
Article