Melatonin treatment ameliorated high-fat diet- and particulate matter-induced cardiac dysfunction, apoptosis, and fibrosis through ROS scavenging and miR-221/222 upregulation.
Does melatonin prevent high-fat diet- and particulate matter-induced cardiac injury in mice?
Melatonin ameliorates cardiac injury induced by combined high-fat diet and particulate matter exposure in mice by reducing mitochondrial ROS and modulating miR-221/222 expression.
) mice were treated with HFD for 4 weeks. PM was injected intratracheally at the end of the second and third weeks, and melatonin 20 mg/kg was administered orally daily starting at the end of the second week. Combined PA/HFD and PM induced mitochondrial ROS accumulation, subsequent mitochondrial fission, and excessive mitophagy in cardiomyocytes and cardiac tissues. This cascade increases cardiomyocyte apoptosis and fibrosis, leading to cardiac dysfunction. Melatonin treatment reduced mitochondrial ROS accumulation and improved HFD- and PM-induced cardiac dysfunction. Further exploration of the molecular mechanism highlighted that miR-221/222 upregulation is a downstream effect of melatonin, revealing a novel regulatory pathway for HFD- and PM-induced cardiac injury. This study showed that simultaneous exposure to HFD/PA and PM exacerbated cardiomyocyte apoptosis and fibrosis. These effects could be ameliorated by melatonin-mediated ROS scavenging, maintenance of mitochondrial function, and cardioprotection associated with miR-221/222.
Chen et al. (Wed,) conducted a other in High-fat diet- and particulate matter-induced cardiac injury. Melatonin was evaluated on Cardiac dysfunction, apoptosis, and fibrosis. Melatonin treatment ameliorated high-fat diet- and particulate matter-induced cardiac dysfunction, apoptosis, and fibrosis through ROS scavenging and miR-221/222 upregulation.