Downregulated MicroRNA-327 Attenuates Oxidative Stress–Mediated Myocardial Ischemia Reperfusion Injury Through Regulating the FGF10/Akt/Nrf2 Signaling Pathway

• Published in: Frontiers in pharmacology 2021-05, Vol.12, p.669146-669146
• Main Authors: Zheng, Tao, Yang, Jun, Zhang, Jing, Yang, Chaojun, Fan, Zhixing, Li, Qi, Zhai, Yuhong, Liu, Haiyin, Yang, Jian
• Format: Article
• Language: English
• Subjects: apoptosis; FGF10; microRNA-327; myocardial ischemia/reperfusion injury; oxidative stress; Pharmacology
• ISSN: 1663-9812; 1663-9812
• DOI: 10.3389/fphar.2021.669146

Although miR-327 had a protective effect on cardiomyocytes as described previously, the potential mechanism still needs further exploration. The aim of this study was to investigate the role and mechanism of miR-327 on oxidative stress in myocardial ischemia/reperfusion injury (MI/RI) process. Oxidative stress and cardiomyocytes injury were detected in rat model of MI/RI, hypoxia/reoxygenation (H/R), and tert-butyl hydroperoxide (TBHP) model of H9c2 cells. In vitro , downregulation of miR-327 inhibited both H/R- and TBHP-induced oxidative stress, and suppressed apoptosis. Meanwhile, fibroblast growth factor 10(FGF10) was enhanced by miR-327 knocked down, followed by the activation of p-PI3K and p -Akt, and the translocation of Nrf2. However, miR-327 overexpression performed with opposite effects. Consistent with the results in vitro , downregulation of miR-327 attenuated reactive oxygen species (ROS) generation as well as intrinsic apoptosis, and alleviated I/R injury. In conclusion, inhibition of miR-327 improved antioxidative ability and myocardial cell survival via regulating the FGF10/Akt/Nrf2 pathway.