| Revista: | Anais da Academia Brasileira de Ciencias |
| Base de datos: | PERIÓDICA |
| Número de sistema: | 000436207 |
| ISSN: | 0001-3765 |
| Autores: | Chen, Quan-Fang1 Wang, Wei1 Huang, Zhou1 Huang, Dong-Ling1 |
| Instituciones: | 1Guangxi Medical University, The First Affiliated Hospital, Nanning, Guanxi. China |
| Año: | 2020 |
| Volumen: | 92 |
| Número: | 1 |
| País: | Brasil |
| Idioma: | Inglés |
| Tipo de documento: | Artículo |
| Enfoque: | Experimental, aplicado |
| Resumen en inglés | To investigated the role of HIF-1α in myocardial inflammatory injury in rats induced by CME and its possible mechanism. Forty SD rats were separated randomly and equally into four groups, i.e. CME+HIF-1α stabilizer dimethyloxalyl glycine (CME+DMOG) group, CME+HIF-1α inhibitor YC-1 (CME+YC-1) group, CME group, and Sham group. HBFP staining, myocardial enzyme assessment, and cardiac ultrasound were used to measure microinfarct, serum c-troponin I (cTnI) level, and Cardiac function. ELISA and western blot were applied for detecting NLRP3 inflammasome pathway and TLR4/MyD88/NF-κB signaling level.Pro-inflammatory factors of IL-18, IL-1β and TNF-α increased their expression levels after CME, which indicated inflammatory responses in the myocardium. Additionally, in the inflammatory process, NLRP3 inflammasome and TLR4/MyD88/NF-κB signaling were involved. DMOG reverses these effects of CME, whereas YC-1 aggravates these effects. HIF-1α may attenuate myocardial inflammatory injury induced by CME and improve cardiac function, which can perhaps be explained by the fact that TLR4/MyD88/NF-κB signaling pathway activation is inhibited |
| Disciplinas: | Medicina |
| Palabras clave: | Medicina experimental, Sistema cardiovascular, Lesión miocárdica inflamatoria, Factor inductor de hipoxia, Inflamasoma |
| Keyword: | Experimental medicine, Cardiovascular system, Myocardial inflammatory injury, Hypoxia-inducible factor, Inflammasome |
| Texto completo: | Texto completo (Ver HTML) Texto completo (Ver PDF) |
