LRG1 expression reduced inflammation of sepsis-renal injury via activation of NLRP3 inflammasome by HIF-1 alpha.

Background: Sepsis is a commonly seen severe case in clinical practice and the main cause of health loss worldwide. Objective: We investigated the biological function of LRG1 and its underlying molecular mechanisms in sepsis-renal injury. Mice of sepsis model group were subjected to cecal ligation and puncture (CLP) surgery after anesthetization. THP-1 cell was induced by LPS for vitro model. Results: The mRNA and protein levels of LRG1 in renal tissue of sepsis model were reduced. LRG1 could reduce the inflammation reaction in model of sepsis-renal injury. In addition, LRG1 up-regulation reduced inflammation reaction and ROS production levels in vitro model via the activation of HIF-1α and suppression of NLRP3 inflammasome. Knockout of LRG1 increased inflammation reaction and ROS production levels in vitro model via the inactivation of HIF-1α and induction of NLRP3 inflammasome. Furthermore, the inhibition of HIF-1α reduced the effects of LRG1 on NLRP3 inflammasome in vitro model. Conclusions: The present study suggests that LRG1 expression reduced inflammation of sepsis-renal injury via activation of NLRP3 inflammasome by HIF-1α, thereby may be a promising therapeutic target of sepsis-renal injury. [ABSTRACT FROM AUTHOR]