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The Phenotypic Conversion of Macrophage Detected by FACS in EAE Mice Treated with or without Fasudil

The Phenotypic Conversion of Macrophage Detected by FACS in EAE Mice Treated with or without Fasudil
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摘要 We studied the changes of macrophage populations in splenic mononuclear cells of experimental autoimmune ence-phalomyelitis (EAE) mice treated with or without Fasudil. Phenotypic analysis using flow cytometry showed that the levels of TLR4, CD11c and CD40 which represent the type 1 macrophage, were depressed in Fasudil-treated mice. Incontrast, it was observed the expressions of CD200 and CD14 which typify the type 2 macrophage were elevated in Fasudil-treated mice as compared to EAE mice. And we also found that Fasudil at dose of 40 mg/kg alleviated the se-verity of symptom in EAE mice. Based on the evidence that M1 macrophages are neurotoxic and M2 macrophages promote a regenerative growth, indicating that polarization and shifting of macrophages into M2 cells may also play key roles in treatment of EAE. We studied the changes of macrophage populations in splenic mononuclear cells of experimental autoimmune ence-phalomyelitis (EAE) mice treated with or without Fasudil. Phenotypic analysis using flow cytometry showed that the levels of TLR4, CD11c and CD40 which represent the type 1 macrophage, were depressed in Fasudil-treated mice. Incontrast, it was observed the expressions of CD200 and CD14 which typify the type 2 macrophage were elevated in Fasudil-treated mice as compared to EAE mice. And we also found that Fasudil at dose of 40 mg/kg alleviated the se-verity of symptom in EAE mice. Based on the evidence that M1 macrophages are neurotoxic and M2 macrophages promote a regenerative growth, indicating that polarization and shifting of macrophages into M2 cells may also play key roles in treatment of EAE.
出处 《Engineering(科研)》 2013年第10期491-495,共5页 工程(英文)(1947-3931)
关键词 Experiment AUTOIMMUNE Excephomeylitis FASUDIL Flow CYTOMETRY MACROPHAGE Experiment Autoimmune Excephomeylitis Fasudil Flow Cytometry Macrophage
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