外泌体是细胞间传递信息的重要载体，具有减轻组织损伤的潜能，也是干细胞旁分泌中最为有效的活性成分之一。迄今对外泌体参与急性肺损伤的作用及其调节机制知之甚少。我们的预实验结果提示脂肪干细胞对脂多糖条件下肺微血管内皮细胞有保护作用。前期研究表明，自噬有助于缺血状态下脂肪干细胞存活及成脂。但脂肪干细胞外泌体在急性肺损伤中的作用及调节机制还有待进一步探讨。为此，我们提出假说：1. 脂肪干细胞外泌体能抑制脂多糖诱发的急性肺损伤炎症，从而减轻肺微血管内皮细胞损伤及凋亡；2.自噬通过调节外泌体合成及分泌参与脂肪干细胞调节急性肺损伤的过程。为了验证这一假说，我们将在细胞和动物水平上，借助多种分子生物学手段，探讨脂肪干细胞外泌体在参与调节急性肺损伤中的作用，明确自噬对外泌体合成及分泌过程的调控机制。本研究将从自噬调控脂肪干细胞外泌体这个新视点为急性肺损伤及其并发症的防治提供新的思路。

Exosome is one of the vital carriers for the transmission of information between cells and the most effective component in stem cells paracrine, and it has been testified the potency in alleviating tissue injury. However, the role and related mechanism of exosome in participating in mediating acute lung injury remain little known. Our previous researches suggested adipose-derived stem cells (ADSCs) play a protective role in lipopolysaccharide-challenging pulmonary microvascular endothelial cells. In addition, we have testified autophagy is helpful in maintaining the ADSCs survival and adipogenesis under ischemia microenvironment. However, it will need be further explored that the role and the related mediating machanism of exosome from ADSCs in acute lng injury. In this light, we hypothesize that 1) exosome from ADSCs could prohibit PMVECs apoptosis and alleviate the pulmonary microvascular endothelial barrier injury through relieving lipopolysaccharide-triggered excessive inflammation；(2 autophagy may regulate the biogenesis and secretion of ADSCs exosomes. For testifying these hypothesis, we will draw support from many a molecular biology method to pursue the role of ADSCs exosomes in lipopolysaccharide-induced acute lung injury, and then further testify how autophagy mediate the biogenesis and secretion of ADSCs exosomes. Our research and findings are helpful of adding new ideas for prevention and treatment acute lung injury and the corresponding complications from the point of autophagy regulating ADSCs exosomes.