Selenium Reduces Lipopolysaccharide-Induced Apoptosis and Oxidative Stress Through the Inhibition of TRPM7 Channel in Neuronal Cells

The trace element selenium (Se) has anti-apoptotic and antioxidant properties. When stimulated by lipopolysaccharide (LPS), brain and neural cells undergo apoptosis and produce reactive oxygen species (ROS). LPS-induced ROS stimulates transient receptor potential melastatin 7 (TRPM7) activation, whereas carvacrol (CRV) and Se inhibit it. The mechanisms by which Se inhibits LPS-induced oxidative stress and apoptosis in neuronal (SH-SY5Y) cells remain unknown. To protect SH-SY5Y cells from ROS-induced apoptosis and death, I investigated how Se alters the TRPM7-mediated molecular pathways. Five main groups were generated in the SH-SY5Y:Control, Se (1 μM for 2 hours), LPS (1 μg/ml for 24 hours), LPS + Se, and LPS + TRPM7 blocker (CRV). Apoptosis, ROS, mitochondrial dysfunction, apoptotic markers (caspase-3, -8, and -9), and cytosolic free Ca2+ were increased by the LPS incubation, whereas Se and CRV treatments reduced these parameters. The LPS decreased cell viability; however, the viability in the LPS + Se and LPS + CRV groups increased with the incubations of Se and CRV.In conclusion, Se decreased LPS-induced oxidative stress and apoptosis by inhibiting TRPM7 in the neuronal cells. One possible treatment agent for oxidative neuronal injury and neurodegenerative disorders induced by LPS could be the Se treatment.