4.5 Article

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

期刊

JOURNAL OF CELLULAR AND MOLECULAR MEDICINE
卷 26, 期 2, 页码 507-514

出版社

WILEY
DOI: 10.1111/jcmm.17108

关键词

acute kidney injury; lipopolysaccharide; podocyte; Toll-like receptor 4

资金

  1. Natural Science Foundation of Jiangsu Province [BK20181150]
  2. Key R&D plan of Xuzhou City

向作者/读者索取更多资源

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

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