MicroRNAs (miRNAs) are short endogenous noncoding RNAs regulating protein translation. However, the specific mechanism by which miR-181b influences sepsis via high-mobility group box-1 protein (HMGB1) still remains unknown. Thus, the aim of this study is to investigate the mechanism of miR-181b in regulating inflammatory response in sepsis-induced myocardial injury through targeting high-mobility group box-1 protein (HMGB1). Through cecal ligation and puncture (CLP), the rat model of sepsis was established. Then, the effect of altered expression of miR-181b and HMGB1 on cardiomyocytes was investigated. The positive expression rate of HMGB1, concentration of inflammatory factors, and serum myocardial enzyme of myocardial tissues were determined. Besides, the binding site between miR-181b and HMGB1 was determined by bioinformatics information and dual-luciferase reporter gene assay. The expression of related genes in cells of each group was determined by RT-qPCR and western blot analysis, and the apoptosis rate of transfected cells in each group was determined by TUNEL assay. HMGB1 expression and inflammatory factors were significantly increased in myocardial tissue of rats with sepsis. Cell morphology and the infiltration of inflammatory cells were significantly improved by overexpression of miR-181b. miR-181b directly targeted HMGB1, and downregulation of HMGB1 reduced inflammatory factors and myocardial injury and inhibited cardiomyocyte apoptosis in sepsis. This present study suggests that miR-181b decreased inflammatory factors and reduced myocardial injury in sepsis through downregulation of HMGB1. Thus, a better understanding of this process may aid in the development of novel therapeutic agents in sepsis.

MicroRNA (miRNA) 是短的内源性非编码 RNA，调节蛋白质翻译。然而，miR-181b 通过高迁移率族框 1 蛋白（HMGB1）影响败血症的具体机制仍然未知。因此，本研究的目的是研究 miR-181b 通过靶向高迁移率组框 1 蛋白 (HMGB1) 在脓毒症诱导的心肌损伤中调节炎症反应的机制。通过盲肠结扎穿刺术（CLP）建立脓毒症大鼠模型。然后，研究了 miR-181b 和 HMGB1 表达改变对心肌细胞的影响。测定心肌组织中HMGB1的阳性表达率、炎症因子浓度和血清心肌酶。除了，miR-181b 与 HMGB1 之间的结合位点是通过生物信息学信息和双荧光素酶报告基因测定确定的。RT-qPCR和Western blot检测各组细胞相关基因的表达，TUNEL法检测各组转染细胞的凋亡率。脓毒症大鼠心肌组织HMGB1表达及炎症因子显着升高。miR-181b的过表达显着改善了细胞形态和炎症细胞的浸润。miR-181b 直接靶向 HMGB1，下调 HMGB1 可减少炎症因子和心肌损伤，并抑制脓毒症中的心肌细胞凋亡。本研究表明，miR-181b 通过下调 HMGB1 减少炎症因子并减少脓毒症中的心肌损伤。因此，更好地了解这一过程可能有助于开发新的脓毒症治疗剂。