Brenner T, Brocke S, Szafer F, Sobel R A, Parkinson J F, Perez D H, Steinman L
Department of Neurology, Hadassah University Hospital, Jerusalem, Israel.
J Immunol. 1997 Mar 15;158(6):2940-6.
Aminoguanidine (AG), a selective inhibitor of inducible nitric oxide synthase, prevented the clinical development of experimental autoimmune encephalomyelitis (EAE) with a reduction in inflammation and demyelination. Administration of AG reduced the expression of nitrosotyrosine in inflammatory lesions in the central nervous system. Cytokine expression, determined by semiquantitative PCR, revealed increased expression of IFN-gamma, IL-10, and TGF-beta, which was associated with protection from EAE, and reduced TNF-alpha, associated with the development of EAE. Furthermore, AG blocked the secretion of nitric oxide, TNF-alpha, and PGE2 in astrocyte cultures. AG did not influence the proliferation response of T cells to a pathogenic epitope of myelin basic protein. Down-regulation of nitric oxide by AG has widespread consequences for cytokine production in central nervous system inflammation and prevents EAE.
氨基胍（AG）是一种诱导型一氧化氮合酶的选择性抑制剂，可通过减轻炎症和脱髓鞘来阻止实验性自身免疫性脑脊髓炎（EAE）的临床进展。给予AG可降低中枢神经系统炎症病变中亚硝基酪氨酸的表达。通过半定量PCR测定的细胞因子表达显示，与EAE保护相关的IFN-γ、IL-10和TGF-β表达增加，而与EAE发展相关的TNF-α表达降低。此外，AG可阻断星形胶质细胞培养物中一氧化氮、TNF-α和PGE2的分泌。AG不影响T细胞对髓鞘碱性蛋白致病表位的增殖反应。AG对一氧化氮的下调对中枢神经系统炎症中的细胞因子产生具有广泛影响，并可预防EAE。
