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
- Natural Science Foundation of Jiangsu Province [BK20181150]
- Key R&D plan of Xuzhou City
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.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据