Melatonin protects H9c2 cardiomyoblasts from oxygen-glucose deprivation and reperfusion-induced injury by inhibiting Rac1/JNK/Foxo3a/Bim signaling pathway.
Cell Biol Int
; 46(3): 415-426, 2022 Mar.
Article
em En
| MEDLINE
| ID: mdl-34882903
ABSTRACT
Melatonin has been shown to protect against ischemia/reperfusion (I/R)-induced myocardial injury, however, the precise molecular mechanisms have not been fully clarified. The present study was aimed to investigate whether inactivation of Rac1/JNK/Foxo3a/Bim signaling pathway is responsible for the protective effect of melatonin on I/R-induced myocardial injury. Our results showed that Foxo3a downregulation contributed to the protective effect of melatonin on OGD/R-induced injury of H9c2 cardiomyoblasts. Melatonin treatment led to a reduced activity of Rac1, which was responsible for Foxo3a downregulation and decreased cell injury in OGD/R-exposed H9c2 cells. Furthermore, JNK acts as a downstream effector of Rac1 in mediating melatonin-induced inactivation of Foxo3a/Bim signaling pathway and decreased cell injury in OGD/R-exposed H9c2 cells. In conclusion, our results indicate that melatonin protects H9c2 cells against OGD/R-induced injury by inactivating the Rac1/JNK/Foxo3a/Bim signaling pathway. This study provided a novel insight into the protective mechanism of melatonin against I/R-induced myocardial injury.
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Texto completo:
1
Base de dados:
MEDLINE
Assunto principal:
Traumatismo por Reperfusão
/
Melatonina
Limite:
Humans
Idioma:
En
Ano de publicação:
2022
Tipo de documento:
Article