The mitochondrial Na+/Ca2+ exchanger may reduce high glucose-induced oxidative stress and nucleotide-binding oligomerization domain receptor 3 inflammasome activation in endothelial cells

摘要: BACKGROUND The mitochondrial Na(+)/Ca(2+) exchanger, NCLX, plays an important role in the balance between Ca(2+) influx and efflux across inner membrane endothelial cells. Mitochondrial metabolism is likely to be affected by activity of NCLX because activates several enzymes Krebs cycle. It currently believed that mitochondria are not only centers energy production but also sites reactive oxygen species (ROS) generation nucleotide-binding oligomerization domain receptor 3 (NLRP3) inflammasome activation. METHODS & RESULTS This study focused on function, rat aortic cells (RAECs), induced glucose. First, we detected increase expression endothelia rats with diabetes mellitus, which was injection streptozotocin. Next, colocalization using confocal analysis. Suppression expression, siRNA construct (siNCLX), enhanced blocked Unexpectedly, silencing increased ROS NLRP3 CONCLUSIONS These findings suggest affects glucose-dependent signaling, thereby regulating activation high glucose conditions. In early stages stimulation, increases compensate order self-protect maintenance, stability, function