脊髓损伤（SCI）后局部炎症反应失调是影响神经功能恢复的主要原因，而巨噬细胞的极化又是主导该炎症反应的关键。最近，对间充质干细胞（MSCs）炎症调节能力的研究改变了人们对MSCs疗法机理的认识。其中，外周血间充质干细胞（PB-MSCs）因具有获取方便等优势而备受关注。预实验中我们发现大鼠PB-MSCs体外能够阻抑因LPS诱导的M0型巨噬细胞向M1型（促炎型）分化，且促进M2型（抗炎型）巨噬细胞分化；该体系中抗炎因子IL-10表达明显升高。我们猜测由IL-10激活的STAT3通路可能为PB-MSCs调控巨噬细胞极化从而主导SCI后炎症反应的重要环节。为此，本研究拟采用大鼠PB-MSCs移植SCI模型，研究其体内外对巨噬细胞不同极化型别及SCI组织炎症反应的调节能力及其机制，探索PB-MSCs的炎症调节可塑性与SCI神经功能恢复的关系，为今后PB-MSCs治疗SCI的临床转化应用提供理论依据。

Overwhelming localized inflammatory reaction is the major obstruction that hinder functional recovery of impaired neurons resulting from spinal cord injuries (SCI). The key factor that govern such reaction is the polarization of macrophages. Recently, researches targeted on the immunomodulatory property of mesenchymal stem cells (MSCs) have changed the view of us on therapies based on MSCs. Among which, peripheral blood-derived MSCs (PB-MSCs) have drawn massive attention for the advantages of their convenience of collection, etc. We discovered that PB-MSCs could suppress the polarization of M0 macrophages towards M1 which induced by LPS in our pre-experiment; the expression of the anti-inflammatory cytokine IL-10 was significantly elevated in the culturing system at the same time. Hence, we presumed that IL-10 together with the STAT3 signal pathways activated by which play a pivotal role in modulating the polarization of macrophages, thereby dominating the progression of inflammatory reaction after SCI. Thus, in this experiment, we decide on transplantation of rats’ PB-MSCs and exploring the mechanism of PB-MSCs modulating the polarization of macrophages and the following inflammation resulted from SCI in vivo and in vitro, so that the relation between the ability of immunomodulation of PB-MSCs and the recovery of neural function after SCI can be revealed. We hope the findings in this research could make foundations for clinical applications of PB-MSCs for curing SCI.