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.
Keywords: HMGB1; Inflammation; Liver injury; Sepsis; miR-103a-3p.