Melatonin alleviated acute myocardial infarction by inhibiting ferroptosis
Authors: HUANG Xiaohui, WEN Weixing, CHEN Peng, LI Weiwen, LI Jiahuan, CAO Yue, HU Yunzhao, HUANG Yuli
AIM: To investigate whether melatonin can ameliorate acute myocardial infarction (AMI) by inhibiting ferroptosis. METHODS: H9C2 cells were cultured in AnaeroPack system with low sugar and serum-free medium for 10 h to construct a cell model of AMI. Then cells were treated with melatonin and ferroptosis inducer erastin. The cell activity, reactive oxygen species (ROS), lipid peroxidation, mitochondrial membrane potential (MMP), and ferroptosis related protein expression were detected. A rat model of AMI induced by isoprenaline (ISO) injection was established to evaluate the effects of melatonin, in which the myocardial infarction size, cardiac injury, pathological changes, oxidative stress, iron ion and ferroptosis related protein expression were examined. RESULTS: Melatonin decreased the oxidative stress, lipid peroxidation and expression of ferroptosis protein in cardiomyocytes induced by hypoxia, but these effects could be impeded by the ferroptosis inducer erastin. Furthermore, in vivo experiments, we also found that melatonin improved the myocardial infarction size, cardiac injury, pathological changes, oxidative stress, and alleviated iron ion accumulation and ferroptosis. CONCLUSION: The cardioprotective effects of melatonin in AMI are associated with the inhibition of ferroptosis.
