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Nitrosporeusine A attenuates sepsis-associated acute kidney injury through the downregulation of IL-6/sIL-6R axis activation-mediated PGC-1α suppression.
- Source :
-
Biochemical & Biophysical Research Communications . Jul2019, Vol. 515 Issue 3, p474-480. 7p. - Publication Year :
- 2019
-
Abstract
- Nitrosporeusine A (NA) has been recently reported to exert anti-inflammatory and renal protective effects, but whether NA can attenuate sepsis-associated acute kidney injury (AKI) has not yet been reported. In this study, our results found that cecal ligation and puncture (CLP) reduced renal PGC-1α expression and induced oxidative stress in C57BL/6 mice. PGC-1α overexpression attenuated CLP-induced AKI with decreased oxidative stress, whereas worsened AKI with excessive reactive oxygen species (ROS) production was observed in renal specific PGC-1α knockout (NiPKO) mice. In addition, PGC-1α expression is retained in IL-6−/− mice and wild-type (WT) C57BL/6 mice received JAK2/STAT3 inhibition. Finally, administration of NA attenuated CLP-induced AKI with decreased IL-6/sIL-6R axis activation, increased PGC-1α expression, and diminished ROS production in injured kidneys. However, NA failed to attenuate CLP-induced AKI in NiPKO mice. Together, these results suggested that NA attenuates sepsis-associated AKI through the downregulation of IL-6/sIL-6R axis activation-mediated renal PGC-1α suppression. • Oxidative stress is a major contributor to the development of CLP-induced AKI in mice. • CLP induces renal oxidative stress through the downregulation of PGC-1α. • IL-6/sIL-6R axis activation is critical for the downregulation of renal PGC-1α in CLP mice. • NA attenuates CLP-induced AKI by reversing IL-6/sIL-6R axis activation-mediated PGC-1α suppression. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 0006291X
- Volume :
- 515
- Issue :
- 3
- Database :
- Academic Search Index
- Journal :
- Biochemical & Biophysical Research Communications
- Publication Type :
- Academic Journal
- Accession number :
- 136980330
- Full Text :
- https://doi.org/10.1016/j.bbrc.2019.05.151