We have previously demonstrated that thyromimetics stimulate oligodendrocyte precursor cell differentiation and promote remyelination in murine demyelination models. We investigated whether a thyroid receptor-beta selective thyromimetic, sobetirome (Sob), and its CNS-targeted prodrug, Sob-AM2, could prevent myelin and axonal degeneration in experimental autoimmune encephalomyelitis (EAE). Compared to controls, EAE mice receiving triiodothyronine (T3, 0.4 mg/kg), Sob (5 mg/kg) or Sob-AM2 (5 mg/kg) had reduced clinical disease and, within the spinal cord, less tissue damage, more normally myelinated axons, fewer degenerating axons and more oligodendrocytes. T3 and Sob also protected cultured oligodendrocytes against cell death. Thyromimetics thus might protect against oligodendrocyte death, demyelination and axonal degeneration as well as stimulate remyelination in multiple sclerosis.

中文翻译：

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甲状腺激素和拟甲状腺素抑制 EAE 中的髓鞘和轴突变性和少突胶质细胞丢失

我们之前已经证明，拟甲状腺素刺激少突胶质细胞前体细胞分化并促进小鼠脱髓鞘模型中的髓鞘再生。我们研究了甲状腺受体-β 选择性拟甲状腺素 (Sob) 及其靶向 CNS 的前药 Sob-AM2 是否可以预防实验性自身免疫性脑脊髓炎 (EAE) 中的髓鞘和轴突变性。与对照组相比，接受三碘甲状腺原氨酸 (T3, 0.4 mg/kg)、Sob (5 mg/kg) 或 Sob-AM2 (5 mg/kg) 的 EAE 小鼠临床疾病减少，脊髓内组织损伤减少，更多正常有髓轴突，退化轴突较少，少突胶质细胞较多。T3 和 Sob 还保护培养的少突胶质细胞免受细胞死亡。因此，拟甲状腺素可以防止少突胶质细胞死亡，