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Cul4a attenuates LPS-induced acute kidney injury via blocking NF-kB signaling pathway in sepsis

Jing Zhao1, Qiuxia Duan2, Cuihong Dong3

  • 1Yantaishan Hospital, Department of Critical Care Medicine, Yantai, China.

Journal of Medical Biochemistry
|May 25, 2022
PubMed
Abstract

Insights

Cul4a protects against septic acute kidney injury (AKI). Upregulating Cul4a reduces oxidative stress, inflammation, and apoptosis in kidney cells by inhibiting the NF-kB pathway.

Area of Science:

  • Nephrology
  • Molecular Biology
  • Pathology

Background:

  • Sepsis-induced acute kidney injury (AKI) is a critical clinical challenge with limited treatment options.
  • AKI can progress to end-stage kidney disease, highlighting the need for effective interventions.
  • The molecular mechanisms underlying septic AKI require further elucidation to identify therapeutic targets.

Purpose of the Study:

  • To investigate the protective role of Cul4a in a septic AKI model.
  • To elucidate the molecular mechanisms by which Cul4a exerts its protective effects in septic AKI.
  • To evaluate Cul4a as a potential therapeutic target for septic AKI.

Main Methods:

  • Established cellular and animal models of septic AKI using lipopolysaccharide (LPS).
  • Assessed Cul4a expression via Western blot and RT-qPCR.
  • Quantified oxidative stress (ROS), inflammation (cytokines, LDH), cell viability (CCK-8), and apoptosis (flow cytometry).
  • Analyzed the NF-kB pathway activation.

Main Results:

  • Cul4a expression was significantly downregulated in septic AKI models.
  • LPS challenge induced oxidative stress, apoptosis, and inflammation, which were ameliorated by Cul4a upregulation.
  • Overexpression of Cul4a inhibited LPS-induced NF-kB pathway activation.
  • Cul4a demonstrated a protective effect against LPS-induced kidney injury.

Conclusions:

  • Cul4a acts as a protective factor in septic AKI.
  • Cul4a mitigates LPS-induced oxidative stress, apoptosis, and inflammation in kidney cells.
  • Inhibition of the NF-kB pathway is a key mechanism underlying Cul4a's protective function in septic AKI.
Keywords:
AKICul4aapoptosisinflammationoxidative stresssepsis

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