Effects of propofol on lipopolysaccharide-induced expression and release of HMGB1 in macrophages

T Wang1, X Y Wei1, B Liu1

  • 1Department of Anesthesiology, the Third Affiliated Hospital, Zhengzhou University, Zhengzhou, China.

Insights

Propofol significantly reduces the expression and release of high-mobility group box 1 protein (HMGB1) in macrophages stimulated by lipopolysaccharide (LPS). This effect is achieved by inhibiting HMGB1 translocation and nuclear factor-kappa B (NF-κB) activity, suggesting a protective role for propofol in sepsis.

Area of Science:

  • Immunology
  • Pharmacology
  • Cell Biology

Background:

  • Sepsis is a life-threatening condition characterized by a dysregulated host response to infection.
  • High-mobility group box 1 protein (HMGB1) is a key inflammatory mediator implicated in sepsis pathogenesis.
  • Lipopolysaccharide (LPS) from Gram-negative bacteria is a potent trigger for inflammatory responses in sepsis.

Purpose of the Study:

  • To investigate the effects of propofol on LPS-induced HMGB1 expression and release in macrophages.
  • To elucidate the underlying mechanisms, including HMGB1 translocation and NF-κB signaling pathway.

Main Methods:

  • Utilized RAW264.7 mouse macrophage cell line.
  • Assessed HMGB1 mRNA and protein levels using RT-PCR and ELISA.
  • Analyzed HMGB1 translocation via Western blotting.
  • Measured NF-κB activity using ELISA.

Main Results:

  • LPS stimulation significantly increased HMGB1 mRNA and protein levels, with translocation from nucleus to cytoplasm.
  • LPS also enhanced nuclear factor-kappa B (NF-κB) activity.
  • Propofol treatment significantly inhibited LPS-induced HMGB1 expression, release, translocation, and NF-κB activity.

Conclusions:

  • Propofol effectively inhibits LPS-induced HMGB1 expression and release in macrophages.
  • Propofol exerts its effects by suppressing HMGB1 translocation and NF-κB activation.
  • These findings suggest propofol possesses potential therapeutic benefits for sepsis patients.