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Inhibition of macrophage migration inhibitory factor (MIF) tautomerase activity suppresses microglia-mediated
Yu Zhang1,2, Ruinan Gu1, Jia Jia1
1Jiangsu Key Laboratory of Translational Research and Therapy for Neuro-Psychiatric Diseases and the Collaborative Innovation Centre for Brain Science, College of Pharmaceutical Sciences, Soochow University, Suzhou, Jiangsu, China.
Abstract:
Macrophage migration inhibitory factor (MIF), a pleiotropic pro-inflammatory cytokine, is a key regulator in both innate and acquired immunity systems. MIF has become a promising drug target for inflammatory diseases. Apart from its cytokine activities, MIF is known to act as a d-dopachrome tautomerase. Our previous work has identified that 3-[(biphenyl-4-ylcarbonyl)carbamothioyl]amino benzoic acid (Z-590) exhibited a potent inhibitory activity against MIF. In this study, we investigate the effect of Z-590 on lipopolysaccharide (LPS)-activated microglial cell activation. Our results demonstrate that Z-590 significantly decreases the production of nitric oxide (NO), tumour necrosis factor-alpha (TNF-α), interleukin (IL)-6, IL-1β, cyclooxygenase (COX-2), inducible nitric oxide synthase (iNOS) as well as reactive oxygen species (ROS) involved in inhibiting MAKPs signalling pathway in LPS-stimulated microglia cells. Furthermore, Z-590 reduced cytotoxicity of activated microglia toward HT-22 hippocampal cells in a microglia-conditioned medium system. Taken together, these results indicate that MIF inhibitor Z-590 elicits a potent inhibitor for microglia-mediated neuroinflammation.
