Multiple sclerosis (MS) is a chronic autoimmune disease characterized by inflammatory infiltration and demyelination in the central nervous system (CNS). Among the factors involved in the immunological mechanisms of MS, T helper 1 (Th1) cells and T helper 17 (Th17) cells play a critical role. Compound 21, a novel phloroglucinol derivative, significantly protected myelin from damage in our previous study. However, it remains unclear whether this compound affects MS. In this study, the experimental autoimmune encephalomyelitis (EAE) rat model was established to mimic the pathological process of MS and evaluate the neuroprotective effect of Compound 21. The results illustrated that Compound 21 treatment notably attenuates neurological deficits, immune infiltration, and demyelination in EAE rats. Our mechanistic investigation revealed that Compound 21 treatment reduces the population of Th1/Th17 cells and inhibits their infiltration into the CNS. Furthermore, we found that the inhibition of Th1/Th17 cell infiltration is related to the direct suppression of Th1/Th17 cell differentiation and the inhibition of proinflammatory microglial cells. Collectively, these results confirm that Compound 21 suppresses infiltrated Th1/Th17 cells to alleviate demyelination in EAE rats, suggesting its potential role as a novel candidate for MS treatment.

中文翻译：

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新型间苯三酚衍生物化合物21通过抑制Th1/Th17细胞浸润保护实验性自身免疫性脑脊髓炎大鼠

多发性硬化症 (MS) 是一种慢性自身免疫性疾病，其特征是中枢神经系统 (CNS) 的炎症浸润和脱髓鞘。在参与 MS 免疫机制的因素中，T 辅助 1 (Th1) 细胞和 T 辅助 17 (Th17) 细胞起着关键作用。在我们之前的研究中，化合物 21 是一种新型间苯三酚衍生物，可显着保护髓鞘免受损伤。然而，尚不清楚这种化合物是否影响 MS。在本研究中，建立实验性自身免疫性脑脊髓炎（EAE）大鼠模型以模拟 MS 的病理过程并评估化合物 21 的神经保护作用。 结果表明化合物 21 治疗显着减轻 EAE 中的神经功能缺损、免疫浸润和脱髓鞘老鼠。我们的机理研究表明，化合物 21 治疗减少了 Th1/Th17 细胞的数量并抑制了它们对中枢神经系统的浸润。此外，我们发现抑制 Th1/Th17 细胞浸润与直接抑制 Th1/Th17 细胞分化和抑制促炎小胶质细胞有关。总的来说，这些结果证实化合物 21 抑制浸润的 Th1/Th17 细胞以减轻 EAE 大鼠的脱髓鞘，表明其作为 MS 治疗的新候选物的潜在作用。