Progranulin (PGRN) is serves as an inflammation-response biomarker and promotes lung damage in burn-induced Sepsis via the SIRT1 Pathways by ROS

Abstract Sepsis has become the focus of research in the field of intensive care medicine due to its high mortality and complicated pathogenesis. To evaluate the effects and mechanism of Progranulin (PGRN) affects inflammation in lung damage of burn-induced Sepsis. In mice of burn-induced Sepsis, PGRN gene expression was increased in lung tissue. So, PGRN promoted inflammation in vitro model through SIRT1/ROS/NLRP3 pathways. Down-regulation of PGRN reduced inflammation via SIRT1/ROS/NLRP3 Pathways. The activation of SIRT1 reduced the effects of PGRN on inflammation in lung cell by LPS via SIRT1/ROS/NLRP3 pathways. The inactivation of NLRP3 decreased the effects of PGRN on inflammation in vitro model. Our data suggest that PGRN is serves as inflammation-response biomarker and promoted lung damage in burn-induced Sepsis via the SIRT1 Pathways by ROS/NLRP3 pathways.