The effects and mechanism of bone marrow stromal cells for spinalcord injury

移植的MSC减轻脊髓损伤后炎症的确切机制仍不清楚。移植的MSC在损伤的脊髓内迁移，没有分化为神经胶质或神经元成分。骨髓间充质干细胞移植与脊髓损伤环境的显著改变有关，IL-4和IL-13水平显著升高，肿瘤坏死因子-α和IL-6水平降低。这与交替激活的巨噬细胞数量增加(M2表型：精氨酸酶-1或CD206阳性)和经典激活的巨噬细胞数量减少(M1表型：iNOS或CD16/32阳性)同时相关。这些变化与MSC移植组的功能运动恢复有关，这与保留轴突、减少瘢痕组织形成和增加髓鞘稀疏有关。我们的结果表明，脊髓损伤后MSC的急性移植通过将巨噬细胞表型从M1转变为M2来改善炎症环境，这可能减少了损伤后亚急性/慢性期抑制性瘢痕组织的影响，为轴突伸展和功能恢复提供了允许的环境。

The precise mechanisms through which transplanted MSC attenuate inflammation after SCI are still unclear. The transplanted MSC migrated within the injured spinal cord without differentiating into glial or neuronal elements. MSC transplantation was associated with marked changes in the SCI environment, with significant increases in IL-4 and IL-13 levels reductions in TNF-α and IL-6 levels. This was associated simultaneously with increased numbers of alternatively activated macrophages (M2 phenotype: arginase -1 or CD206-positive) and decreased numbers of classically activated macrophages (M1 phenotype: iNOS or CD16/32-positive). These changes were associated with functional locomotion recovery in the MSC transplanted group, which correlated with preserved axons, less scar tissue formation and increased myelin sparring. Our results suggested that acute transplantation of MSC after SCI modified the inflammatory environment by shifting the macrophage phenotype from M1 to M2, and that this may reduce the effects of the inhibitory scar tissue in the subacute/chronic phase after injury to provide a permissive environment for axonal extension and functional recovery.