肝移植是终末期肝病唯一有效的治疗方法，缺血再灌注损伤是影响其死亡率的重要因素。血栓素A2主要由肝非实质细胞（包括肝星状细胞，肝血管内皮细胞和库普弗细胞）分泌，最新的研究证明其是机体抗感染的重要因子并参与肝脏缺血再灌注损伤。我们的前期研究发现：实验组小鼠饮用水中添加广谱抗生素可以显著降低缺血再灌注之后的肝脏损伤程度。从小鼠肝脏中提取原代肝非实质细胞的实验结果表明：仅库普弗细胞在特异性的Toll样受体激动剂刺激下血栓素A2水平显著性升高，而在其他细胞中未见此现象。因此，我们推测：抗生素预处理能通过巨噬细胞表面Toll样受体调控血栓素A2水平保护小鼠缺血再灌注损伤。进一步通过构建环氧化酶（COX-1）基因缺陷小鼠以及人原代肝脏巨噬细胞的实验验证，我们将探索血栓素A2及巨噬细胞参与肝缺血再灌注损伤过程的崭新机制。这可能是将来治疗肝缺血再灌注损伤的潜在靶点，并为围手术期处理提供新的治疗手段或思路。

Liver transplantation is the only effective treatment for end-stage liver diseases, ischemia-reperfusion injury (IRI) significantly affects mortality in liver transplant patients. Thromboxane (TX) A2, mainly secreted by liver non-parenchymal cells (including hepatic stellate cells, hepatic vascular endothelial cells, and Kupffer cells), has been recently identified as an important factor of bacterial defense and participated in the process of IRI. In pre-experiments, we found that treating mice in the experimental group with broad-spectrum antibiotics can significantly reduce the liver injury after IRI. The experimental results of primary liver non-parenchymal cells extracted from mouse liver showed that only Kupffer cells significantly increased the levels of thromboxane A2 under the stimulation of specific Toll-like receptor (TLR) agonists. Therefore, we hypothesized that antibiotic pretreatment protects mice from hepatic IRI by regulating TXA2 levels through TLRs on the surface of Kupffer cells. Further by constructing cyclooxygenase (COX-1) gene-deficient mice and extracting human primary Kupffer cells and conducting experiments, we may explore a new mechanism of thromboxane A2 and macrophages involved in the process of liver IRI. This may be a potential target for the treatment of hepatic IRI in the future, and provide new treatments or ideas for perioperative management of liver transplantation.