脓毒症相关急性肾损伤(SA-AKI)死亡率高，但机制未明确。细胞焦亡在AKI中起重要作用。MФ 与肾小管上皮细胞（TECs）通过交互作用影响SA-AKI进程。我们发现：M1、M2型巨噬细胞与TECs共培养，M1型加重细胞焦亡，M2型减轻细胞焦亡；M1、M2型巨噬细胞分泌的外泌体与TECs共培养，M1型加重细胞焦亡，M2型减轻细胞焦亡；miR-93在M1中低表达，在M2中高表达；细胞焦亡通路相关蛋白TXNIP是miR-93的靶基因。因此我们提出假说：MФ 分化的M1、M2不同表型可导致AKI细胞功能差异；M2外泌体中高表达的miR-93可抑制细胞焦亡。本课题将利用芯片筛选、生物信息学分析和细胞功能验证等方法，从体外细胞分子、体内动物实验水平阐明通过外泌体介导的miR-93-TXNIP-NLRP3细胞焦亡导致M1及M2型巨噬细胞在脓毒症相关急性肾损伤中功能差别的机制，为AKI治疗提供新思路。

The mortality of sepsis-associated acute kidney injury (SA-AKI) is high, but the mechanism is not clear. Pyroptosis plays an important role in AKI. MФ interacts with renal tubular epithelial cells (TECs) to influence the SA-AKI process. We found that when M1 and M2 macrophages were co-cultured with TECs, M1 type aggravated pyroptosis, M2 type attenuated pyroptosis. When M1 and M2 macrophages secreted exosomes were co-cultured with TECs, M1 type aggravated pyroptosis, the M2 type attenuated pyroptosis. The miR-93 was lowly expressed in M1 type and highly expressed in M2 type. The pyroptosis related protein TXNIP was the miR-93 target gene. Therefore, we propose a hypothesis: MФ differentiated M1 and M2 phenotypes may lead to functional differences in AKI cells. The miR-93, which is highly expressed in M2 type exosomes, inhibits pyroptosis. This project will use microarray screening, bioinformatics analysis, cell function verification and other methods to elucidate the functional difference of M1 and M2 macrophages in sepsis-associated acute kidney injury induced by exosomes-mediated miR-93-TXNIP-NLRP3 pyroptosis via in vitro cellular and in vivo animal experiments. This mechanism study will provide new ideas for AKI treatment.