Therapeutic Effects of Benzoylacetonitrile on Microglia Activation in Multiple Sclerosis

Background:
 Multiple Sclerosis (MS) is an autoimmune disease of the central nervous system (CNS). Pathogenic T cells, such as Th1 and Th17, infiltrate CNS, resulting in neuroinflammation, demyelination axonal damage. activates microglia (MG) CNS Th17 acts a chemokine to recruit immune cells into CNS. MG resident cell its activation associated with destruction myelin secretion inflammatory cytokines IL-12, IL-23 IL-1β. IL-12 are important for differentiation reactivation, respectively. IL-1β key mediator response. Benzoylacetonitrile (BTN) has been shown reduce severity mouse model MS vitro. However, effects BTN on unknown, this study was aimed investigate We hypothesize that can suppress decrease production cytokines.
 Methods:
 Primary were pretreated at concentration 200μM or 300μM 2 hours DMSO (vehicle), followed by lipopolysaccharide (LPS) 100ng/ml stimulation 1.5 3 hours. RNA isolated from mRNA expression levels IL-23, measured using Q-PCR.
 Results:
 Our results showed suppressed reduced cytokine production. The LPS BTN-treated significantly lower than LPS-treated MG.Conclusion: This demonstrated able vitro, suggesting exhibits immunomodulatory potential attenuate neuroinflammation through reduction Conclusion:
 cytokines.