The liver is one of the most vulnerable organs during sepsis. Current studies have proven that microRNAs play important roles in injury and inflammation. The current study aimed to investigate the role of miR-103 in septic liver injury. The sepsis model was established by cecal ligation and puncture in mice. Then, the mice were divided into four groups: normal group, sepsis group, sepsis + miR-103a-3p agomir group, and sepsis + negative control group. Liver injury was observed by hematoxylin-eosin staining and electron microscopic studies. The sepsis-induced apoptosis in liver tissues was assessed by TUNEL staining. The levels of inflammatory cytokines in liver tissues were determined by enzyme-linked immunosorbent assay kits. The targeted gene of miR-103a-3p in cells was predicted by bioinformatics algorithm and confirmed by dual-luciferase reporter assay. The expression of miR-103a-3p, HMBG1, and the apoptosis-relative proteins was examined by quantitative real-time polymerase chain reaction and Western blotting. miR-103a-3p was downregulated in liver tissues of sepsis animals. miR-103a-3p agomir could alleviate liver injury including the tissue injury and mitochondrial damage, inhibit the secretion of inflammatory factors, and decrease the apoptosis of liver cells. The high-mobility group B1 (HMGB1) was overregulated in sepsis, and it was a downstream target gene of miR-103a-3p. The results of the rescue assay confirmed that miR-103a-3p had a protection role in septic liver injury by targeting HMGB1. In summary, HMGB1 was one of the genes targeted by miR-103a-3p, which played roles in septic injury. These data may provide novel insight for the identification of new target and treatment strategies for septic liver injury.

肝脏是脓毒症期间最脆弱的器官之一。目前的研究已经证明，microRNAs 在损伤和炎症中发挥着重要作用。本研究旨在探讨 miR-103 在脓毒性肝损伤中的作用。小鼠盲肠结扎穿刺建立脓毒症模型。然后将小鼠分为四组：正常组、脓毒症组、脓毒症+miR-103a-3p agomir组、脓毒症+阴性对照组。通过苏木精-伊红染色和电子显微镜研究观察肝损伤。通过 TUNEL 染色评估脓毒症诱导的肝组织细胞凋亡。通过酶联免疫吸附测定试剂盒测定肝组织中炎性细胞因子的水平。通过生物信息学算法预测细胞中miR-103a-3p的靶向基因，并通过双荧光素酶报告基因测定确认。通过定量实时聚合酶链反应和蛋白质印迹检测 miR-103a-3p、HMBG1 和凋亡相关蛋白的表达。miR-103a-3p 在脓毒症动物的肝组织中下调。miR-103a-3p agomir可以减轻包括组织损伤和线粒体损伤在内的肝损伤，抑制炎症因子的分泌，减少肝细胞的凋亡。高迁移率组 B1 (HMGB1) 在脓毒症中被过度调节，它是 miR-103a-3p 的下游靶基因。抢救试验结果证实，miR-103a-3p通过靶向HMGB1对脓毒性肝损伤具有保护作用。总之，HMGB1 是 miR-103a-3p 靶向的基因之一，它在脓毒性损伤中起作用。这些数据可能为确定脓毒性肝损伤的新靶点和治疗策略提供新的见解。