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首页> 外文期刊>Cellular immunology >Atorvastatin ameliorates experimental autoimmune neuritis by decreased Th1/Th17 cytokines and up-regulated T regulatory cells.
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Atorvastatin ameliorates experimental autoimmune neuritis by decreased Th1/Th17 cytokines and up-regulated T regulatory cells.

机译：阿托伐他汀通过减少Th1 / Th17细胞因子和上调T调节细胞来改善实验性自身免疫性神经炎。

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摘要

Statins have anti-inflammatory and immune-regulating properties. To investigate the effects of atorvastatin on experimental autoimmune neuritis (EAN), an animal model of Guillain-Barre syndrome (GBS), atorvastatin was administered to Lewis rats immunized with bovine peripheral myelin in complete Freund's adjuvant. We found that atorvastatin ameliorated the clinical symptoms of EAN, decreased the numbers of inflammatory cells as well as IFN-gamma(+) and IL-17(+) cells in sciatic nerves, decreased the CD80 expression and increased the number of CD25(+)Foxp3(+) cells in mononuclear cells (MNC), and decreased the levels of IFN-gamma in MNC culture supernatants. These data provide strong evidence that atorvastatin can act as an inhibitor in EAN by inhibiting the immune response of Th1 and Th17, decreasing the expression of co-stimulatory molecule, and up-regulating the number of T regulatory cells. These data demonstrated that statins could be used as a therapeutic strategy in human GBS in future.
机译：他汀类药物具有抗炎和免疫调节特性。为了研究阿托伐他汀对实验性自身免疫性神经炎（EAN）（吉兰-巴雷综合征（GBS）的动物模型）的影响，将阿托伐他汀用于完全弗氏佐剂中牛外周血髓磷脂免疫的Lewis大鼠。我们发现阿托伐他汀改善了EAN的临床症状，减少了坐骨神经炎性细胞以及IFN-γ（+）和IL-17（+）细胞的数量，降低了CD80的表达并增加了CD25（+）的数量）单核细胞（MNC）中的Foxp3（+）细胞，并降低了MNC培养上清液中的IFN-γ水平。这些数据提供了有力的证据，证明阿托伐他汀可以通过抑制Th1和Th17的免疫反应，减少共刺激分子的表达以及上调T调节细胞的数量而充当EAN的抑制剂。这些数据表明，他汀类药物将来可以用作人类GBS的治疗策略。

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