Melatonin protects H9c2 cardiomyoblasts from oxygen‐glucose deprivation and reperfusion‐induced injury by inhibiting Rac1/JNK/Foxo3a/Bim signaling pathway. (16th December 2021)

• Record Type: Journal Article
• Authors: Wang, Yulin; Jian, Ying; Zhang, Xiaofu; Ni, Bin; Wang, Mingwei; Pan, Chunqi
• Is Part Of: Cell biology international. Volume 46:Number 3(2022)
• Page Start: 415
• Page End: 426
• Publication Date: 2021-12-16
• Subjects: cardiomyocytes -- FOXO3a -- ischemia–reperfusion injury -- JNK -- melatonin -- Rac1; Cytology -- Periodicals; Cells -- Periodicals; 571.605
• DOI: 10.1002/cbin.11739
• Languages: English
• ISSNs: 1065-6995

Abstract

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.