Tacrolimus alleviates LPS‐induced AKI by inhibiting TLR4/MyD88/NF‐κB signalling in mice

• DOI: 10.1111/jcmm.17108
• Publication Date: 2021-12-10T05:31:56Z
• Authors: Xueqing Hu; Wenqian Zhou; Shun Wu; Rui Wang; Zhiyong Luan; Xin Geng; Na Xu; Zhaoyong Zhang; Zhenmin Ruan; Zenghui Wang; Furong Li; Chen Yu; Hongqi Ren
• Keywords: Lipopolysaccharides; Toll-Like Receptor 4; 0301 basic medicine; Mice; 03 medical and health sciences; Myeloid Differentiation Factor 88; NF-kappa B; Animals; Original Articles; Acute Kidney Injury; Tacrolimus; 3. Good health

Abstract Lipopolysaccharide (LPS)‐induced sepsis‐associated acute kidney injury (SA‐AKI) is a model of clinical serious care syndrome, with high morbidity and mortality. Tacrolimus (TAC), novel immunosuppressant that inhibits inflammatory response, plays pivotal role in diseases. In this study, LPS treated mice cultured podocytes were used as the models SA‐AKI vivo vitro , respectively. Medium‐ high‐dose TAC administration significantly attenuated renal function pathological manifestations at 12, 24 48 h after treatment mice. Moreover, Toll‐like receptor 4 (TLR4)/myeloid differential protein‐88 (MyD88)/nuclear factor‐kappa (NF‐κB) signalling pathway was also dramatically inhibited by medium‐ addition, reversed LPS‐induced podocyte cytoskeletal migratory capability. Our findings indicate has protective effects against AKI inhibiting TLR4/MyD88/NF‐κB dysfunction, providing another potential therapeutic for SA‐AKI.