Nerve demyelination or axonal lesions are characteristic of experimental autoimmune neuritis (EAN). Previous studies have demonstrated that microRNA-338 can regulate the differentiation and maturation of oligodendrocytes and Schwann cells and promote injured peripheral nerves in rats. In this study, we used microRNA-338 coded lentivirus vector (miR-338-LV) in a Lewis rat EAN model, in with the conjunction P0 peptide 180–199 which was injected into the footpads of animals to induce immunization. The clinical scores of miR-338-LV and intravenous immunoglobulin (IVIg) (positive drug) groups were significantly superior to those of untreated group at disease peak and disease plateau (p < 0.05). The nerve conduction velocity and the compound nerve action potential amplitude of miR-338-LV and IVIg groups increased significantly compared to those of the untreated group at disease peak (p < 0.01). At disease peak, myelin swelling, cavity formation, and lamellae separation showed improvement in miR-338-LV and IVIg groups compared to untreated group. S100 and NF200 expression in miR-338-LV and IVIg groups increased compared to that in untreated group. Iba1 and S100 co-expression in Schwann cells in miR-338-LV and IVIg groups decreased compared to that in untreated group, which was indicative of the reduced conversion of Schwann cells into inflammatory cells. Overall, miR-338-LV in sciatic nerves might improve neuromuscular function in EAN by inhibiting the conversion of Schwann cells into inflammatory cells.

神经脱髓鞘或轴突病变是实验性自身免疫性神经炎 (EAN) 的特征。先前的研究表明，microRNA-338可以调节少突胶质细胞和雪旺细胞的分化和成熟，促进大鼠周围神经损伤。在这项研究中，我们在 Lewis 大鼠 EAN 模型中使用了 microRNA-338 编码的慢病毒载体 (miR-338-LV)，结合 P0 肽 180-199，将其注射到动物的足垫中以诱导免疫。miR-338-LV和静脉注射免疫球蛋白（IVIg）（阳性药物）组的临床评分在疾病高峰期和疾病平台期显着优于未治疗组（p < 0.05)。miR-338-LV和IVIg组的神经传导速度和复合神经动作电位幅度较未治疗组在疾病高峰期显着增加（p < 0.01)。在疾病高峰期，与未治疗组相比，miR-338-LV 和 IVIg 组的髓鞘肿胀、空洞形成和薄片分离显示出改善。与未治疗组相比，miR-338-LV 和 IVIg 组中 S100 和 NF200 的表达增加。与未处理组相比，miR-338-LV 和 IVIg 组雪旺细胞中 Iba1 和 S100 的共表达降低，这表明雪旺细胞向炎性细胞的转化减少。总的来说，坐骨神经中的 miR-338-LV 可能通过抑制雪旺细胞向炎症细胞的转化来改善 EAN 中的神经肌肉功能。