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  2. Schisantherin A attenuates sepsis-induced acute kidney injury by suppressing inflammation via regulating the NRF2 pathway

Schisantherin A attenuates sepsis-induced acute kidney injury by suppressing inflammation via regulating the NRF2 pathway

  • Life Sci. 2020 Oct 1;258:118161. doi: 10.1016/j.lfs.2020.118161.
Yuan Gui 1 Youjing Yang 2 Deyu Xu 3 Shasha Tao 4 Jianzhong Li 5
Affiliations

Affiliations

  • 1 Division of Nephrology, Department of Medicine, University of Iowa Carver College of Medicine, Iowa City, IA 52242, United States of America.
  • 2 School of Public Health, Medical College of Soochow University, 199 Ren'ai Road, Suzhou 215123, Jiangsu, China.
  • 3 Department of Nephrology, The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu 215006, China.
  • 4 School of Public Health, Medical College of Soochow University, 199 Ren'ai Road, Suzhou 215123, Jiangsu, China. Electronic address: taoqishu619@126.com.
  • 5 Department of Nephrology, The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu 215006, China. Electronic address: ljzsnk@hotmail.com.
Abstract

Aims: Tubulointerstitial inflammation is recognized as a key determinant of progressive sepsis-induced acute kidney injury (AKI). Schisantherin A (SchA) has been shown to be capable of regulating inflammatory processes. In the present study, we explored the possibility of SchA in preventing lipopolysaccharide (LPS)-induced kidney inflammation and injury.

Materials and methods: AKI was induced by a single intraperitoneal injection of LPS in CD1 mice, administration of SchA was used for treatment. The protective effect of SchA on renal function and inflammation were analyzed respectively; the NRK-52E cell line was employed for the in vitro study and relative molecular mechanism was explored.

Key findings: Administration with SchA markedly attenuated LPS-induced damage on renal function and histopathological changes of the kidney. Additionally, pretreatment with SchA could inhibit the expression of inflammatory factors in the kidneys. In NRK-52E cells, SchA treatment significantly inhibited LPS-induced NF-κB activation and pro-inflammatory cytokine expression. Moreover, SchA could promote NRF2 pathway activation, and further blockade of NRF2 activation reversed the SchA-induced inhibition of NF-κB activation.

Significance: These presented results indicated that SchA may have great potential for protecting against sepsis-induced AKI.

Keywords

Acute kidney injury; Inflammation; Lipopolysaccharide; NRF2; Schisantherin A.

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