脓毒症急性肾损伤（AKI）是重症医学常见的问题，死亡率高，其机制尚不清楚。研究发现Galectin-3在多种炎症疾病中通过激活TLR4炎症通路，诱导炎性因子大量释放，进而导致组织损伤。我们近期研究发现Galectin-3在脓毒症早期升高，且峰值时间早于IL-6和血肌酐，通过特异性清除Galectin-3，可减轻AKI，改善预后。但其在脓毒症AKI中的机制尚不明确。我们假设：在脓毒症中，Galectin-3可通过激活TLR4，诱导肾小管上皮细胞中促炎信号的释放，从而导致AKI的发生。本研究拟通过脓毒症AKI患者及动物模型，验证Galectin-3对AKI的预测作用；利用肾小管上皮细胞和基因敲除小鼠，从TLR4和细胞促炎通路，阐明Galectin-3参与脓毒症AKI发生的分子机制。本研究对进一步阐明脓毒症AKI的发生机制，寻找脓毒性AKI新的治疗靶点具有重要的科学意义。

Septic acute kidney injury (AKI) is the most common problem in ICU with increased mortality and healthcare costs. However, its pathophysiology remains poorly understood. Galectin-3, a member of the galectin family, expressed in epithelial and endothelial cells, plays a multi-functional role with a broad range of activities such as promotion of neutrophil adhesion and production of pro-inflammatory cytokines in various tissue injuries by binding to and activating Toll-like receptor 4. Our previous studies showed that serum and urine Galectin-3 concentration increased at 2 hours in rats undergoing sepsis induced by cecal ligation and puncture (CLP)，and removal Galectin-3 with specific adsorptive material could attenuated septic AKI. But the precise role of Galectin-3 in pathogenesis of septic AKI is still unknown. Based on the findings, we hypothesized that: in septic AKI, Galectin-3 acts as an endogenous ligand to induce pro-inflammatory cytokines in renal tubular epithelial cells by activating TLR4. This study will explore the mechanism of Galectin-3 in septic AKI by in vitro cell experiments and Galectin-3-null mice. The study is of great significance on the illustration of the pro-inflammatory mechanism of Gal-3 in pathogenesis of septic AKI, and provides potential therapeutic targets.