游离脂肪是最理想的软组织填充剂，但其高吸收率是限制了其广泛临床应用。究其原因，关键在于缺乏对其存活及再生机制的深入了解。课题组前期研究发现，脂肪再生是游离脂肪移植后体积保留的核心机制，并且发现PGE2介导的炎症反应是脂肪再生过程中重要的调节因素。通过干预COX2-PGE2环路调控脂肪移植的免疫微环境可影响脂肪移植的结局，而这一过程与髓系来源免疫抑制细胞（MDSCs）密切相关。本研究拟探讨PGE2对MDSCs的增殖或功能的影响，观察游离移植后脂肪组织内MDSCs与炎症水平的关系，并通过调控移植物中PGE2的水平观察MDSCs对游离脂肪移植保留率的影响这三部分内容，阐明MDSCs与脂肪存活/再生的密切相关性。本研究将进一步揭示游离脂肪移植后的脂肪再生的炎症调控模式, 并为通过调节脂肪移植后中的PGE2水平来诱导游离脂肪移植物的再生提供理论依据。

Autologous fat should be considered as the most ideal soft tissue filler; however，it suffered from high absorption rate. Thus, a thorough understanding onthe survival and regeneration mechanism of fat grafting is required. Our previous studies have found that adipose tissue regeneration is the key process after free fat transplantation. Moreover, the inflammation mediated by prostaglandin E2(PGE2) played an important role in the regulation of the fat tissue regeneration in fat grafting. By observing the tissue slice of the transferred fat, we accidentally found a structure closely related to the early inflammation, which was identified as myeloid derived stem cells(MDSCs). This study intends to.investigate the role of MDSCs on immune cells and adipose stem cells, to characterize the relation between MDSCs and the inflammation activity in the fat grafts and to observe the influence of MDSCs on fat graft retention rate by depletion of the MDSCs in the fat grafts, expounding the close relationship between the MDSCs and fat graft survival / regeneration. This study will further reveal the inflammatory regulation mode after free fat transplantation, and provide a theoretical basis for guiding improving the fat graft retention rate by.adjusting the level of PGE2 after fat transplantation.