骨髓间充质干细胞（BM-MSCs）在急性肺损伤（ALI）的修复中扮演重要角色，但其参与ALI损伤修复发生机制仍不甚明了。本课题组前期工作已证实：BM-MSCs通过旁分泌核心蛋白聚糖（DCN）上调ALI自噬相关关键基因Beclin-1与LC3B的水平，提高ALI自噬水平，从而显著减轻ALI的损伤严重程度。为此，我们提出假说：BM-MSCs可能通过分泌DCN正向调控ALI的自噬水平从而发挥其损伤修复的作用。为此，我们建立小鼠急性肺损伤及人肺微血管内皮细胞损伤模型；培养BM-MSCs并收集BM-MSCs的条件培养基；采用siRNA干涉抑制或慢病毒载体转染改变BM-MSCs中DCN的表达，进一步检测BM-MSCs中不同DCN水平对ALI自噬水平及损伤修复能力的变化，从分子、细胞及整体水平等探讨BM-MSCs发挥修复ALI的作用机制，为临床寻找BM-MSCs治疗ALI提供新的理论依据。

Bone marrow-derived mesenchymal stem cells (BM-MSCs) appear to exert an important therapeutic effect in acute lung injury (ALI). However, the underlying mechanism triggered by BM-MSCs is unclear up until now. Preliminary work from our research group has already confirmed that BM-MSCs can significantly up-regulate the levels of autophagy related genes-Beclin-1 and LC3B by paracrine decorin (DCN) and increase the level of autophagy in ALI, which significantly reduced the severity of ALI. Thus we speculate BM-MSCs can trigger the level of autophagy by DCN to reduce the severity of ALI. On the basis of established model of ALI mice and human pulmonary microvascular endothelial cells (HPMVECs), the BM-MSCs or conditioned medium of BM-MSCs were cultured and collected and then used siRNA interference to suppress or transfected with virus vector to up regulate the expression of DCN. Furthermore, according to the different levels of DCN expression in BM-MSCs, the effects of BM-MSCs on ALI and autophagy were investigated to explore the mechanism underlying this process at the molecular, cellular, and animal levels. It also provides the theoretical evidence for finding new therapeutic target point in ALI.