脓毒症肠屏障功能障碍是危重患者继发多脏器功能障碍的主要原因之一，其发病机制尚未完全阐明。肠屏障功能依赖于肠上皮细胞增殖与凋亡的动态平衡。前期研究发现PLK1在调控肠上皮细胞凋亡与增殖平衡中发挥关键作用。脓毒症时炎症因子释放激活NF-κB信号通路，诱导肠上皮细胞凋亡。预实验发现抑制PLK1可以激活NF-κB信号通路。既往研究提示PLK1与TANK存在直接联系。因此课题组推测PLK1通过与TANK相互作用调控NF-κB信号通路活性在脓毒症肠屏障功能障碍中发挥作用。本项目拟在前期研究基础上，通过构建脓毒症模型，在动物水平和细胞水平探讨PLK1-TANK-NF-κB信号通路在脓毒症肠屏障功能障碍调控中的作用及分子机制，为脓毒症肠屏障功能障碍的防治提供新思路和策略。

Sepsis-induced intestinal barrier dysfunction is a critical reason for multiple organ dysfunction in critically ill patients, while the pathogenesis is not yet fully elucidated. Intestinal barrier function depends on the balance between proliferation and apoptosis of intestinal epithelial cell. We found that PLK1 plays a key role in regulating the balance of intestinal epithelial cell apoptosis and proliferation. During sepsis, the release of inflammatory cytokines activated NF-κB signaling pathway, leading to the apoptosis of intestinal epithelial cells. Preliminary experiments found that inhibiting PLK1 activated the NF-κB signaling pathway. Previous studies suggested that PLK1 and TANK have a direct interaction.Therefore, we speculate that PLK1 plays a critical role in sepsis-induced intestinal barrier dysfunction by interacting with TANK to regulate the activity of NF-κB signaling pathway. To verify this hypothesis, we will mimic the sepsis model in vivo and in vitro to explore the role and mechanism of PLK1-TANK-NF-κB signaling pathway in sepsis induced intestinal barrier dysfunction. This project will provide a new idea and strategy for the treatment of sepsis-induced intestinal barrier.