Edaravone Inhibits Inflammation in Toll-Like Receptor 4-Stimulated PBMNCs from Multiple Sclerosis Patients

Background: Multiple sclerosis (MS) is a neurological disorder that is directly linked to inflammation in the central nervous system (CNS). The activation of toll-like receptors (TLRs) exacerbates neuroinflammation by increasing the production of reactive oxygen species (ROS) and proinflammatory cytokines. Edaravone (EDV) has been proposed as a potential therapy for CNS diseases because of its free radical scavenging and anti-inflammatory properties. This study investigated the effects of EDV on the inflammatory response in TLR4-stimulated peripheral blood mononuclear cells (PBMNCs) from MS patients and a healthy control group. Methods: The impact of EDV on ROS production in lipopolysaccharide (LPS)-stimulated PBMNCs was assessed using the 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyl-2H-tetrazolium bromide (MTT) reduction and luminol-dependent chemiluminescence assays. The interleukin (IL)-6 concentration in the PBMNC supernatants was measured using enzyme-linked immunosorbent assay (ELISA). Results: The results showed that ROS production in PBMNCs stimulated using LPS (a TLR4 activator) was significantly inhibited (p < 0.05) by EDV in the MS patients and control group. Additionally, EDV significantly reduced IL-6 secretion in TLR4-stimulated PBMNCs in these groups (p < 0.05). No significant differences were observed between the groups. Conclusion: Our findings suggest that EDV may serve as an adjunctive therapy for MS by reducing ROS and IL-6 production in TLR4-stimulated PBMNCs in MS patients, highlighting its potential in modulating neuroinflammation and oxidative stress.