Little is known regarding the functional role of microRNA-193-3p (miR-193-3p) in sepsis. Hence, the aim of the present study was to investigate the effect of miR-193-3p on myocardial injury in mice with sepsis and its mechanism through the regulation of signal transducers and activators of transcription 3 (STAT3). The mice model of sepsis was established by cecal ligation and puncture (CLP), septic mice were injected with miR-193-3p agomir, miR-193-3p antagomir or siRNA-STAT3. The expression of miR-193-3p, STAT3 and HMGB1 in the myocardial tissue of septic mice were detected. Cardiac ultrasound, hemodynamics, myocardial injury markers, inflammatory factors and cardiomyocyte apoptosis in septic mice were measured. MiR-193-3p expression was reduced while STAT3 expression was increased in septic mice. Down-regulated STAT3 or up-regulated miR-193-3p improved cardiac function, attenuated myocardial injury, inflammation and cardiomyocyte apoptosis in septic mice. Knockdown STAT3 reversed the role of inhibited miR-193-3p for mice with sepsis. miR-193-3p targeted STAT3, thereby inhibiting HMGB1 expression. This study provides evidence that miR-193-3p targets STAT3 expression to reduce HMGB1 expression, thereby reducing septic myocardial damage. MiR-193-3p might be a potential candidate marker and therapeutic target for sepsis.

中文翻译：

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microRNA-193-3p通过STAT3/HMGB1轴减轻脓毒症小鼠心肌损伤

关于 microRNA-193-3p (miR-193-3p) 在脓毒症中的功能作用知之甚少。因此，本研究的目的是通过调节信号转导和转录激活因子 3 (STAT3) 来研究 miR-193-3p 对脓毒症小鼠心肌损伤的影响及其机制。采用盲肠结扎和穿刺(CLP)方法建立脓毒症小鼠模型，给脓毒症小鼠注射miR-193-3p agomir、miR-193-3p antagomir或siRNA-STAT3。检测脓毒症小鼠心肌组织中miR-193-3p、STAT3和HMGB1的表达。测定脓毒症小鼠的心脏超声、血流动力学、心肌损伤标志物、炎症因子和心肌细胞凋亡。MiR-193-3p 表达减少，而 STAT3 表达在脓毒症小鼠中增加。下调 STAT3 或上调 miR-193-3p 可改善脓毒症小鼠的心脏功能，减轻心肌损伤、炎症和心肌细胞凋亡。敲低 STAT3 逆转了抑制 miR-193-3p 对脓毒症小鼠的作用。miR-193-3p 靶向 STAT3，从而抑制 HMGB1 表达。该研究提供了证据表明 miR-193-3p 靶向 STAT3 表达以降低 HMGB1 表达，从而减少脓毒性心肌损伤。MiR-193-3p 可能是脓毒症的潜在候选标志物和治疗靶点。该研究提供了证据表明 miR-193-3p 靶向 STAT3 表达以降低 HMGB1 表达，从而减少脓毒性心肌损伤。MiR-193-3p 可能是脓毒症的潜在候选标志物和治疗靶点。该研究提供了证据表明 miR-193-3p 靶向 STAT3 表达以降低 HMGB1 表达，从而减少脓毒性心肌损伤。MiR-193-3p 可能是脓毒症的潜在候选标志物和治疗靶点。