RP105 exerts hepatoprotective effects in sepsis by modulating the SOCS2/JAK2/STAT3 signaling pathway

During the occurrence of sepsis, the liver plays a crucial role in immune defense. However, the excessive immune response within the liver can also make it the main target organ for sepsis-related injuries. In this paper, our aim is to explore the protective role of RP105 in liver injury caused by sepsis and clarify its underlying molecular mechanisms. We established a cecal ligation and puncture (CLP) model using RP105 knockout mice. We observed the protective effect of RP105 on liver damage caused by sepsis. We also conducted RNA sequencing (RNA-Seq) analysis on the CLP group and the RP105 knockout CLP group. Furthermore, through in vitro and in vivo experiments, we found that RP105 alleviated liver injury caused by sepsis through the classical regulation of SOCS2 via the JAK2/STAT3 signaling pathway. To investigate the role of RP105 in sepsis-induced liver injury, we employed both in vivo and in vitro approaches. An in vivo mouse model of sepsis was established using the cecal ligation and puncture (CLP) technique. RP105 knockout (RP105⁻/⁻) mice and wild-type (WT) littermates were subjected to CLP surgery, and liver tissues were harvested 24 hours post-surgery for histological and molecular analyses. To elucidate the molecular mechanisms underlying the protective effects of RP105, RNA sequencing (RNA-Seq) was performed on liver samples from WT-CLP and RP105⁻/⁻-CLP groups (n=3 per group).