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MnTBAP treatment ameliorates aldosterone-induced renal injury by regulating mitochondrial dysfunction and NLRP3

Xiao Bi1, Jingjing Wang1, Yuqing Liu1

  • 1Division of Nephrology, Shanghai Ninth People's Hospital, School of Medicine, Shanghai Jiaotong University 639 Zhizaoju Road, Shanghai 200011, China.

American Journal of Translational Research
|January 22, 2019
PubMed

Insights

MnTBAP protects against kidney damage caused by aldosterone by improving mitochondrial function and reducing inflammation. This study shows MnTBAP is a potential therapeutic for aldosterone-induced renal injury.

Area of Science:

  • Nephrology
  • Biochemistry
  • Cell Biology

Background:

  • Aldosterone contributes to chronic kidney disease (CKD) pathogenesis by damaging renal tubular cells.
  • Current treatments for aldosterone-induced renal injury remain limited.

Purpose of the Study:

  • To investigate the protective effects of MnTBAP against aldosterone-induced renal tubular injury.
  • To explore MnTBAP's mechanisms in vitro and in vivo.

Main Methods:

  • Utilized HK-2 cells and aldosterone-infused mice models.
  • Assessed mitochondrial DNA (mtDNA) expression, mitochondrial membrane potential (MMP), cell apoptosis, and NLRP3 inflammasome activation.
  • Evaluated renal tubular cell apoptosis and phenotypic alterations in vivo.

Main Results:

  • MnTBAP treatment ameliorated mitochondrial dysfunction (decreased mtDNA and MMP) in HK-2 cells.
  • MnTBAP reduced aldosterone-induced cell apoptosis and phenotypic alterations in HK-2 cells.
  • MnTBAP inhibited NLRP3 inflammasome activation and pro-inflammatory cytokine release (IL-1β, IL-18).
  • In vivo, MnTBAP improved mitochondrial morphology and function, suppressed NLRP3 inflammasome, reduced renal tubular cell apoptosis, and ameliorated renal injury.

Conclusions:

  • MnTBAP demonstrates significant protective effects against aldosterone-induced renal injury.
  • MnTBAP exerts its protective role by modulating mitochondrial dysfunction and the NLRP3 inflammasome signaling pathway.
Keywords:
AldosteroneMnTBAPNLRP3 inflammasomemitochondrial dysfunction

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