Edaravone Inhibits the Production of Reactive Oxygen Species in Phagocytosis- and PKC-Stimulated Granulocytes from Multiple Sclerosis Patients Edaravone Modulate Oxidative Stress in Multiple Sclerosis

Abstract

Background: Oxidative stress is associated with the pathogenesis of MS. Edaravone (EDV) has been proposed as a therapeutic resource for central nervous system diseases, and it was effective in reducing oxidative stress. However, the antioxidant mechanisms of EDV are poorly studied. Objective: This study aimed to evaluate the effects of EDV on resting, phagocytosis, and PKC-activated granulocytes derived from MS patients and a healthy control group. Methods: The effects of EDV on ROS production in phagocytosis (ROS production in the presence of opsonized particles) and PKC-stimulated granulocytes were evaluated in a luminol-dependent chemiluminescence method. Calphostin C was used in some experiments to compare with those of EDV. Results: EDV inhibited ROS production in phagocytosis of opsonized particles and PKC-stimulated granulocytes from MS patients and healthy control group. In the presence of calphostin C, the inhibition of ROS production was similar to that observed with EDV. Conclusion: These findings suggest the involvement of EDV on the ROS-PKC-NOX signaling pathways modulating oxidative stress in MS. EDV represents a promising treatment option to control oxidative innate immune response for MS.