METRNL reduced inflammation in sepsis-induced renal injury via PPARδ-dependent pathways

• Autor(a) principal: HU,Jin
• Data de Publicação: 2022
• Outros Autores: HE,Aiting, YUE,Xiaolin, ZHOU,Minmin, ZHOU,Yanhong
• Tipo de documento: Artigo
• Idioma: eng
• Título da fonte: Food Science and Technology (Campinas)
• Texto Completo: http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0101-20612022000100772
• topic: METRNL; PPARδ; sepsis; renal injury; inflammation

Abstract Sepsis is a systemic inflammatory response syndrome (SIRS) caused by infection, with complicated pathological mechanism and extremely high prevalence and fatality rate. In this study, we investigated the role of METRNL in sepsis-induced renal injury and to identify potential downstream molecules. Male C57BL/6 mice were subjected to laparotomy followed by extracorporeal cecum mobilization and ligation as vivo model. THP-1 cells were stimulated with LPS as vitro model. As compared to the normal tissue or normal serum samples, the tissue and serum of METRNL expression levels in sepsis-induced renal injury were reduced. METRNL protein reduced inflammation and inhibited renal injury in sepsis mice model. METRNL up-regulation inhibited inflammation in vitro model. The inhibition of METRNL promoted inflammation and renal injury in sepsis mice model. METRNL reduced inflammation in sepsis-induced renal injury via PPARδ-dependent pathways. In conclusion, we are the first to identify METRNL as a co-activator of PPARδ to inhibit inflammation in sepsis-induced renal injury and potentiate the activity target of renal injury.