脊髓缺血再灌注损伤是胸腹主动脉瘤手术的严重并发症，七氟烷对SCIRI有保护作用。前期发现SCIRI时脊髓TUG1增加，miR-29降低，七氟烷抑制TUG1，增加miR-29，TUG1可结合并负性调控miR-29，推测脑脊液exosomes内SP1结合并正向调控脊髓TUG1。推测SCIRI时七氟烷抑制SP1高表达和TUG1高表达，增加miR-29，负性调控TRAF3-Smac/DIABLO-caspase3、BMF-Bax-caspase3和TRIL-TLR4-IL-1β通路保护脊髓神经元。本项目先验证SP1与TUG1结合作用；再验证miR-29与TRAF3、BMF和TRIL结合作用，再研究七氟烷预处理对氧糖剥夺神经元和SCIRI时SP1、TUG1、miR-29及TRAF3、BMF和TRIL基因表达和功能影响，最后探讨七氟烷、SP1抑制剂、TUG1抑制剂、miR-29对SCIRI的保护作用。

Spinal cord ischemia-reperfusion injury (SCIRI) is one of the most serious complications of thoracic abdominal aneurysm surgery. Sevoflurane has a protective effect on SCIRI but the mechanism is unclear. In the early stage, it was found that TUG1 increased and miR-29 decreased in spinal cord tissue suffered by SCIRI,，while sevoflurane inhibited TUG1 and increased miR-29. Previous experiments confirmed that TUG1 could bind to miR-29 and negatively regulate miR-29, and predicted that SP1 might be related to TUG1 ，combined with positive regulation of TUG1 changes. Cerebrospinal fluid contains a variety of cell-derived exosomes, which may be involved in SCIRI by carrying SP1-mediated spinal neurons injury. Based on a series of preliminary research, we speculated that sevoflurane suppressed the expression of SP1 in exosomes of cerebrospinal fluid and TUG1 while increased miR-29 in spinal cord neurons suffered by SCIRI, further inhibited the pathway of TRAF3-Smac/DIABLO-caspase3, BMF-Bax-caspase3 and TRIL-TLR4-IL-1 to protect spinal neurons. This study was first to confirm the binding and regulation of SP1 in exosomes of cerebrospinal fluid and TUG1 in spinal cord. Secondly，to confirm the direct effect and binding site of miR-29 and TRAF3, BMF and TRIL, We also investigated the expression and function of SP1 in exosomes of cerebrospinal fluid 、TUG1, miR-29 and TRAF3, BMF and TRIL in spinal cord on the pretreatment of sevoflurane in the oxygen glucose deprivation of models of neurons，In the end，we tend to explore the protective effects of sevoflurane, SP1 inhibitor, TUG1 inhibitor, miR-29 alone or combination in SCIRI.