Tanshinone IIA ameliorates myocardial ischemia/reperfusion injury in rats by regulation of NLRP3 inflammasome activation and Th17 cells differentiation
Acta cir. bras
; 37(7): e370701, 2022. graf, ilus
Article
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| LILACS, VETINDEX
| ID: biblio-1402968
Biblioteca responsable:
BR68.1
ABSTRACT
Purpose:
Tanshinone IIA is a well-known lipophilic active constituent refined from traditional Chinese medicines, danshen. It has been previously demonstrated to possess various biological properties, including anti-inflammatory, antioxidant, promoting angiogenesis effect and so on. However, the mechanism of tanshinone IIA on myocardial ischemia-reperfusion injury (MI/RI) remains unclear. In this study, we investigated the effect of tanshinone IIA on MI/RI.Methods:
MI/RI rat models were set up. Echocardiographic evaluation and hematoxylin and eosin staining were performed to analyze the cardiac function and morphology of MI/RI. Western blot was conducted for the detection of protein expression of pyrin domain containing 3 (NLRP3) and caspase-1 in heart tissues. Flow cytometry and real-time polymerase chain reaction were used for the detection of proinflammatory cytokines and Th17 cells differentiation.Results:
We found that tanshinone IIA alleviated the myocardial damage of MI/RI, ameliorated the overall and local inflammatory reaction, and produced a cardioprotective effect by inhibiting of NLRP3 inflammasome activation and Th17/Treg cells differentiation.Conclusions:
Our results highlighted the cardio-protective effect of tanshinone IIA on MI/RI and uncovered its underlying mechanism related to the NLRP3 inflammasome inhibition and the modulation of Th17/Treg cells differentiation.Palabras clave
Texto completo:
1
Índice:
LILACS
Asunto principal:
Daño por Reperfusión Miocárdica
/
Isquemia Miocárdica
/
Salvia miltiorrhiza
/
Células Th17
/
Proteína con Dominio Pirina 3 de la Familia NLR
Límite:
Animals
Idioma:
En
Revista:
Acta cir. bras
Asunto de la revista:
CIRURGIA GERAL
/
Procedimentos Cir£rgicos Operat¢rios
Año:
2022
Tipo del documento:
Article