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  3. Research Domains
  5. Biomedical And Clinical Sciences
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  11. Inhibiting Caspase-3/gsdme-mediated Pyroptosis Ameliorates Septic Lung Injury In Mice Model.
  1. Home
  3. Research Domains
  5. Biomedical And Clinical Sciences
  7. Oncology And Carcinogenesis
  9. Predictive And Prognostic Markers
  11. Inhibiting Caspase-3/gsdme-mediated Pyroptosis Ameliorates Septic Lung Injury In Mice Model.

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Inhibiting caspase-3/GSDME-mediated pyroptosis ameliorates septic lung injury in mice model.

Hongqian Qin1, Na Lu1, Kai Chen1

  • 1Department of Respiratory and Critical Care Medicine, the First Affiliated Hospital of Bengbu Medical University, China; Anhui Province Key Laboratory of Clinical and Preclinical Research in Respiratory Disease, China; Clinical Research Center for Respiratory Disease (tumor) in Anhui Province, 287 Changhuai Road, Anhui 233004, China.

Molecular Immunology
|July 2, 2024

View abstract on PubMed

Summary
This summary is machine-generated.

Sepsis-induced acute lung injury involves caspase-3/gasdermin-E (GSDME)-mediated pyroptosis. Inhibiting either caspase-3 or GSDME in mice models significantly alleviates lung injury, suggesting therapeutic potential.

Keywords:
Caspase-3GSDMEPyroptosisSepsis induced lung injury

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Area of Science:

  • Cellular Biology
  • Pathology
  • Immunology

Background:

  • Sepsis is a critical illness with acute lung injury as a severe complication.
  • Pyroptosis, a programmed cell death, is implicated in various inflammatory diseases.

Purpose of the Study:

  • To investigate the role of caspase-3/gasdermin-E (GSDME)-mediated pyroptosis in sepsis-induced lung injury.
  • To evaluate the therapeutic potential of inhibiting caspase-3 or GSDME in a mouse model.

Main Methods:

  • A mouse model of sepsis-induced lung injury was established using cecal ligation and puncture (CLP).
  • Lung injury was assessed via lung coefficient, H&E staining, and electron microscopy.
  • Caspase-3 and GSDME activity, inflammatory markers (LDH, IL-6, IL-18, IL-1β), and protein expression were measured.
  • Specific inhibitors for caspase-3 (Z-DEVD-FMK) and GSDME (AC-DMLD-CMK) were administered.

    • Main Results:

    • CLP-induced sepsis led to increased cleaved-caspase-3 and GSDME-N terminal expression, lung structural damage, and elevated LDH, IL-6, IL-18, and IL-1β levels.
    • Treatment with caspase-3 or GSDME inhibitors ameliorated lung injury and reduced inflammatory markers.
    • Inhibition of caspase-3 or GSDME effectively suppressed pyroptosis.

    Conclusions:

    • Caspase-3/GSDME-mediated pyroptosis plays a crucial role in the pathogenesis of sepsis-induced lung injury.
    • Targeting caspase-3 or GSDME presents a promising therapeutic strategy for sepsis-induced lung injury.