Abstract
Sepsis-induced cardiac injury is associated with oxidative stress and mitochondrial dysfunction. Docosahexaenoic acid (DHA), an essential omega-3 fatty acid, protects the injured myocardium by modulating mitochondrial dysfunction. We aimed to confirm whether the cardioprotective effect of DHA is mediated via the alleviation of mitochondrial fragmentation in lipopolysaccharide (LPS)-induced cardiomyopathy in vitro. We found that DHA improved cell viability and alleviated cardiac cell apoptosis by reducing lactate dehydrogenase (LDH) release, expression levels of Cleaved caspase-3, and Caspase 3 activity. DHA attenuated oxidative stress as evidenced by decreased ROS production and increased superoxide dismutase activity. In addition, DHA ameliorated mitochondrial dysfunction by modulating mitochondrial respiratory chain injury and mitochondrial fragmentation, especially decreasing the mitochondrial fission-related protein p-Drp1(ser 616) but no effects on Drp1, p-Drp1(ser 637), and mitochondrial fusion-related protein. Our data suggest that DHA conferred cardioprotection by alleviating oxidative stress-induced apoptosis, which may be associated with alleviation of stress-induced mitochondrial fragmentation.