Biochanin A attenuates myocardial ischemia/reperfusion injury through the TLR4/NF-κB/NLRP3 signaling pathway
Acta cir. bras; 34 (11), 2019
Publication year: 2019
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.
Antiinflamatorios/farmacología, Aspartato Aminotransferasas/sangre, Western Blotting, Cardiotónicos/farmacología, Creatina Quinasa/sangre, Citocinas/sangre, Genisteína/farmacología, Lactato Deshidrogenasas/sangre, Daño por Reperfusión Miocárdica/metabolismo, Daño por Reperfusión Miocárdica/prevención & control, FN-kappa B/efectos de los fármacos, FN-kappa B/metabolismo, Proteína con Dominio Pirina 3 de la Familia NLR/efectos de los fármacos, Ratas Sprague-Dawley, Valores de Referencia, Reproducibilidad de los Resultados, Transducción de Señal/efectos de los fármacos, Receptor Toll-Like 4/efectos de los fármacos, Receptor Toll-Like 4/metabolismo