Tuyển tập báo cáo các nghiên cứu khoa học quốc tế ngành hóa học dành cho các bạn yêu hóa học tham khảo đề tài: Oral administration of the KATP channel opener diazoxide ameliorates disease progression in a murine model of multiple sclerosis | Virgili et al. Journal of Neuroinflammation 2011 8 149 http content 8 1 149 JJOURNAL1 OF. NEUROINFLAMMATION RESEARCH Open Access Oral administration of the KATP channel opener diazoxide ameliorates disease progression in a murine model of multiple sclerosis 1t 1t 1 1 2 Noemí Virgili Juan F Espinosa-Parrilla Pilar Mancera Andrea Pasten-Zamorano Javier Gimeno-Bayon Manuel J Rodríguez2 Nicole Mahy2 and Marco Pugliese1 2 Abstract Background Multiple Sclerosis MS is an acquired inflammatory demyelinating disorder of the central nervous system CNS and is the leading cause of nontraumatic disability among young adults. Activated microglial cells are important effectors of demyelination and neurodegeneration by secreting cytokines and others neurotoxic agents. Previous studies have demonstrated that microglia expresses ATP-sensitive potassium KATP channels and its pharmacological activation can provide neuroprotective and anti-inflammatory effects. In this study we have examined the effect of oral administration of KATP channel opener diazoxide on induced experimental autoimmune encephalomyelitis EAE a mouse model of MS. Methods Anti-inflammatory effects of diazoxide were studied on lipopolysaccharide LPS and interferon gamma IFNg -activated microglial cells. EAE was induced in C57BL 6J mice by immunization with myelin oligodendrocyte glycoprotein peptide MOG35-55 . Mice were orally treated daily with diazoxide or vehicle for 15 days from the day of EAE symptom onset. Treatment starting at the same time as immunization was also assayed. Clinical signs of EAE were monitored and histological studies were performed to analyze tissue damage demyelination glial reactivity axonal loss neuronal preservation and lymphocyte infiltration. Results Diazoxide inhibited in vitro nitric oxide NO tumor necrosis factor alpha TNF-a and interleukin-6 IL-6 production and inducible nitric oxide synthase iNOS expression by activated microglia without affecting .
