Biochanin A attenuates myocardial ischemia/reperfusion injury through the TLR4/NF-κB/NLRP3 signaling pathway
Acta cir. bras
; Acta cir. bras;34(11): e201901104, Nov. 2019. graf
Article
em En
| LILACS
| ID: biblio-1054677
Biblioteca responsável:
BR1.1
ABSTRACT
Abstract Purpose:
Myocardial ischemia/reperfusion (Ml/R) injury is a leading cause of damage in cardiac tissues, with high rates of mortality and disability. Biochanin A (BCA) is a main constituent of Trifolium pratense L. This study was intended to explore the effect of BCA on Ml/R injury and explore the potential mechanism.Methods:
In vivo MI/R injury was established by transient coronary ligation in Sprague-Dawley rats. Triphenyltetrazolium chloride staining (TTC) was used to measure myocardial infarct size. ELISA assay was employed to evaluate the levels of myocardial enzyme and inflammatory cytokines. Western blot assay was conducted to detect related protein levels in myocardial tissues.Results:
BCA significantly ameliorated myocardial infarction area, reduced the release of myocardial enzyme levels including aspartate transaminase (AST), creatine kinase (CK-MB) and lactic dehydrogenase (LDH). It also decreased the production of inflammatory cytokines (IL-1β, IL-18, IL-6 and TNF-α) in serum of Ml/R rats. Further mechanism studies demonstrated that BCA inhibited inflammatory reaction through blocking TLR4/NF-kB/NLRP3 signaling pathway.Conclusion:
The present study is the first evidence demonstrating that BCA attenuated Ml/R injury through suppressing TLR4/NF-kB/NLRP3 signaling pathway-mediated anti-inflammation pathway.Palavras-chave
Texto completo:
1
Coleções:
01-internacional
Base de dados:
LILACS
Assunto principal:
Cardiotônicos
/
Traumatismo por Reperfusão Miocárdica
/
NF-kappa B
/
Genisteína
/
Receptor 4 Toll-Like
/
Proteína 3 que Contém Domínio de Pirina da Família NLR
Tipo de estudo:
Evaluation_studies
Limite:
Animals
Idioma:
En
Revista:
Acta cir. bras
Assunto da revista:
Cirurgia Geral
/
Procedimentos Cir£rgicos Operat¢rios
Ano de publicação:
2019
Tipo de documento:
Article
País de afiliação:
China
País de publicação:
Brasil