sq-23377 has been researched along with Encephalitis* in 2 studies
2 other study(ies) available for sq-23377 and Encephalitis
| Article | Year |
|---|---|
A Lecinoxoid, an oxidized phospholipid small molecule, constrains CNS autoimmune disease.
Oxidized phospholipids (Ox-PLs) are generated in abundance at sites of inflammation. Recent studies have indicated that Ox-PLs may also exhibit anti-inflammatory activities. In this study, we investigated the beneficial effect of VB-201, a pure synthetic Ox-PL analog that we synthesized, on the development of a central nervous system (CNS) autoimmune inflammatory disease, in vivo. Oral administration of VB-201 ameliorated the severity of experimental autoimmune encephalomyelitis (EAE) induced by myelin oligodendrocyte glycoprotein (MOG) peptide MOG35-55, and restrained the encephalogenicity of MOG35-55-specific T-cells. Our data presents a novel prospect for the role of Ox-PL analogs in CNS inflammatory diseases. Topics: Animals; Bone Marrow Cells; Bromodeoxyuridine; CD4 Antigens; Cell Differentiation; Central Nervous System; Cytokines; Dendritic Cells; Disease Models, Animal; Drug Interactions; Encephalitis; Encephalomyelitis, Autoimmune, Experimental; Enzyme-Linked Immunosorbent Assay; Female; Forkhead Transcription Factors; Freund's Adjuvant; Glycerylphosphorylcholine; Glycoproteins; Ionomycin; Ionophores; Lymph Nodes; Mice; Mice, Inbred BALB C; Mice, Inbred C57BL; Myelin-Oligodendrocyte Glycoprotein; Peptide Fragments; Pertussis Toxin; Phosphorylcholine; Polymethacrylic Acids; Severity of Illness Index; T-Lymphocytes; Time Factors | 2010 |
Lipopolysaccharide sensitizes microglia toward Ca(2+)-induced cell death: mode of cell death shifts from apoptosis to necrosis.
Little is known about the effect of microglial activation on cell death. This study examines the effects of lipopolysaccharide (LPS) and interferon-gamma (IFN-gamma), triggers of microglial activation, on cell death induced by several agents in cultured rat microglia. For comparison, the effect of LPS on cell death is also examined in cultured astrocytes. LPS or IFN-gamma enhanced cell death induced by thapsigargin or ionomycin, an agent that increases intracellular Ca2+ concentration, although LPS or IFN-gamma alone did not affect cell viability. Thapsigargin or ionomycin induced apoptosis in LPS-untreated microglia, while they induced necrosis in LPS-treated microglia, which were partially reversed by O,O'-bis(2-aminophenyl)ethyleneglycol-N,N,N',N'-tetraacetic acid tetraacetoxymethyl ester (BAPTA-AM, an intracellular Ca2+ chelator). In contrast, LPS treatment did not affect tunicamycin- or staurosporine-induced apoptosis, while it inhibited S-nitroso-N-acetylpenicillamine-induced apoptosis. The effect of LPS on thapsigargin or ionomycin-induced apoptosis was not observed in astrocytes. These results indicate that microglial activation sensitizes the cells toward cell death induced by the change in intracellular Ca2+ concentration and shifts the mode of cell death from apoptosis to necrosis. Topics: Animals; Animals, Newborn; Apoptosis; Astrocytes; Calcium; Calcium Signaling; Cells, Cultured; Drug Interactions; Egtazic Acid; Encephalitis; Gliosis; Inflammation Mediators; Interferon-gamma; Intracellular Fluid; Ionomycin; Lipopolysaccharides; Microglia; Necrosis; Rats; Rats, Wistar; S-Nitroso-N-Acetylpenicillamine; Thapsigargin | 2006 |