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Effect of dexmedetomidine on kidney injury in sepsis rats through TLR4/MyD88/NF-κB/iNOS signaling pathway

Y-H Jin1, Z-T Li, H Chen

  • 1Department of Critical Care Medicine, Nanfang Hospital, Southern Medical University, Guangzhou, China. 35793407@qq.com.

European Review for Medical and Pharmacological Sciences
|June 19, 2019
PubMed
Abstract

Insights

Dexmedetomidine (DEX) protects against sepsis-induced acute kidney injury (AKI) in rats. DEX treatment inhibits the Toll-like receptor 4 (TLR4)/MyD88/NF-κB/iNOS pathway, reducing kidney damage and inflammation.

Area of Science:

  • Nephrology
  • Pharmacology
  • Immunology

Background:

  • Sepsis-induced acute kidney injury (AKI) is a critical complication with high mortality.
  • The Toll-like receptor 4 (TLR4) signaling pathway plays a key role in sepsis-related kidney damage.
  • Targeting inflammatory pathways offers a potential therapeutic strategy for AKI.

Purpose of the Study:

  • To investigate the protective effects of dexmedetomidine (DEX) on lipopolysaccharide (LPS)-induced AKI in rats.
  • To elucidate the underlying mechanism involving the TLR4/MyD88/NF-κB/iNOS signaling pathway.

Main Methods:

  • Establishment of an LPS-induced sepsis rat model.
  • Administration of DEX to the treatment group.
  • Assessment of kidney function via serum creatinine and blood urea nitrogen levels.
  • Measurement of pro-inflammatory cytokines (IL-6, IL-1β, TNF-α) and anti-inflammatory cytokine (IL-10) using ELISA.
  • Histopathological examination of kidney tissues using HE staining.
  • Quantification of TLR4, MyD88, NF-κB, and iNOS mRNA and protein expression via qPCR and Western blotting.

Main Results:

  • LPS-induced sepsis caused significant kidney injury, elevated serum creatinine and BUN, increased pro-inflammatory cytokines, and upregulated TLR4/MyD88/NF-κB/iNOS pathway components.
  • DEX treatment markedly improved kidney function and attenuated kidney tissue damage.
  • DEX administration significantly reduced the levels of pro-inflammatory cytokines and downregulated the expression of TLR4, MyD88, NF-κB, and iNOS.

Conclusions:

  • Dexmedetomidine exhibits a significant protective effect against LPS-induced AKI in rats.
  • The mechanism of DEX's protective action is associated with the inhibition of the TLR4/MyD88/NF-κB/iNOS signaling pathway.

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