炎症是缺血性急性肾损伤中重要的病理生理改变，其主要免疫细胞反应包括：中性粒细胞趋化聚集、树突状细胞活化、调节性T细胞功能减退。miR-181家族具有抑制多种细胞增殖、促进细胞凋亡、调节T淋巴细胞增生分化与发育、抑制炎症等功能。在肾脏缺氧缺血早期，miR-181d表达显著下降。为此，我们提出假说：高表达miR-181d可能通过抑制中性粒细胞的聚集、减轻树突状细胞的活化、改善调节性T细胞功能，减轻肾损伤早期炎症进程。为了验证这一假说，我们构建肾损伤分子1启动子调控的miR-181d表达载体，采用慢病毒载体转染、原位杂交等手段，探讨miR-181d在缺血性AKI肾组织损伤和炎症反应中的作用，明确miR-181d通过抑制中性粒细胞聚集、减轻树突细胞活化、改善调节性T细胞功能，减轻肾损伤后炎症反应，保护肾组织的潜在机制。本研究将探讨miR-181d 对缺血性急性肾损伤后炎症的改善作用。

Inflammation is one of the most important pathophysiological changes in acute ischemic renal injury, its main immune cell responses include neutrophil chemotaxis, dendritic cell activation and regulatory T cells dysfunction. The miR-181 family has a number of functions such as inhibition of cell proliferation, promotion of cell apoptosis, regulation of T lymphocyte proliferation and differentiation, as well as inhibition of inflammation. The expression of miR-181d decreased significantly in the early stage of renal hypoxia-ischemia. Therefore, we hypothesized that the high expression of miR-181d may attenuate early inflammatory processes in renal injury by inhibiting neutrophil aggregation, reducing dendritic cell activation, and improving regulatory T cell function. To test this hypothesis, we will construct the miR-181d expression vector regulated by the kidney injury molecule 1 promoter, using several methods such as lentiviral vector transfection, in situ hybridization, and Western blot, to explore the role of miR-181d on ischemic injury and inflammation in renal tissue of AKI, discuss whether miR-181d could alleviate the inflammatory reaction and protect the renal tissue after renal injury by inhibiting the aggregation of neutrophils, reducing the activation of dendritic cells and improving the function of regulatory T cells. This study will investigate the ameliorative effect of miR-181d in inflammation after acute ischemic renal injury.