Circular RNA (circRNA) has been shown to play an important function in the progression of human diseases, including sepsis with acute kidney injury (AKI). However, the role and mechanism of circ_0091702 in sepsis-induced AKI have yet to be confirmed. Lipopolysaccharide (LPS) was used to induce HK2 cells to construct AKI cell models in vitro. Quantitative real-time PCR was used to measure the expression of circ_0091702, inflammatory cytokines, microRNA (miR)-545-3p and thrombospondin 2 (THBS2). Cell counting kit 8 assay and flow cytometry were used to assess cell viability and apoptosis. Besides, the protein levels of apoptosis markers and THBS2 were evaluated by western blot analysis. In addition, the concentrations of inflammatory cytokines were detected by enzyme-linked immunosorbent assay (ELISA). Cell oxidative stress was determined by detecting the contents of oxidative stress markers. Dual-luciferase reporter assay and RIP assay were used to confirm the relationship between miR-545-3p and circ_0091702 or miR-545-3p and THBS2. Circ_0091702 was downregulated in septic AKI patients and LPS-induced HK2 cells. Circ_0091702 could attenuate LPS-induced HK2 cell injury, while its silencing had an opposite effect. In the terms of mechanism, circ_0091702 could act as a sponge of miR-545-3p, and miR-545-3p could directly target THBS2. Functional experiments revealed that miR-545-3p could reverse the alleviating effect of circ_0091702 on LPS-induced HK2 cell injury, and THBS2 knockdown also could overturn the suppressing effect of miR-545-3p inhibitor on LPS-induced HK2 cell injury. Additionally, we also suggested that circ_0091702 could sponge miR-545-3p to regulate THBS2 expression. In conclusion, our results showed that circ_0091702 could suppress LPS-induced HK2 cell injury via the miR-545-3p/THBS2 axis, indicating that circ_0091702 might be an important biomarker for relieving sepsis-related AKI.

环状 RNA (circRNA) 已被证明在人类疾病的进展中发挥重要作用，包括急性肾损伤 (AKI) 的脓毒症。然而，circ_0091702在脓毒症诱导的AKI中的作用和机制尚未得到证实。采用脂多糖（LPS）诱导HK2细胞体外构建AKI细胞模型。采用实时定量 PCR 检测circ_0091702、炎性细胞因子、microRNA ( miR ) -545-3p和血小板反应蛋白 2 ( THBS2 ) 的表达。细胞计数试剂盒 8 测定和流式细胞术用于评估细胞活力和细胞凋亡。此外，细胞凋亡标志物和THBS2的蛋白水平通过蛋白质印迹分析评估。此外，通过酶联免疫吸附试验（ELISA）检测炎性细胞因子的浓度。通过检测氧化应激标志物的含量来确定细胞氧化应激。双荧光素酶报告基因检测和 RIP 检测用于确认miR-545-3p与circ_0091702或miR-545-3p与THBS2之间的关系。Circ_0091702在脓毒症 AKI 患者和 LPS 诱导的 HK2 细胞中下调。Circ_0091702可以减轻 LPS 诱导的 HK2 细胞损伤，而其沉默具有相反的效果。在机制方面，circ_0091702可以充当海绵miR-545-3p和miR-545-3p可以直接靶向THBS2。功能实验表明，miR-545-3p可以逆转circ_0091702对LPS诱导的HK2细胞损伤的缓解作用， THBS2敲低也可以逆转miR-545-3p抑制剂对LPS诱导的HK2细胞损伤的抑制作用。此外，我们还建议circ_0091702可以海绵miR-545-3p来调节THBS2的表达。总之，我们的结果表明，circ_0091702可以通过miR-545-3p / THBS2抑制 LPS 诱导的 HK2 细胞损伤。轴，表明circ_0091702可能是缓解脓毒症相关 AKI 的重要生物标志物。