Mexenone protects mice from LPS-induced sepsis by EC barrier stabilization

PLoS One. 2024 May 9;19(5):e0302628. doi: 10.1371/journal.pone.0302628. eCollection 2024.

Abstract

Blood vessels permit the selective passage of molecules and immune cells between tissues and circulation. Uncontrolled inflammatory responses from an infection can increase vascular permeability and edema, which can occasionally lead to fatal organ failure. We identified mexenone as a vascular permeability blocker by testing 2,910 compounds in the Clinically Applied Compound Library using the lipopolysaccharide (LPS)-induced vascular permeability assay. Mexenone suppressed the LPS-induced downregulation of junctional proteins and phosphorylation of VE-cadherin in Bovine Aortic Endothelial Cells (BAECs). The injection of mexenone 1 hr before LPS administration completely blocked LPS-induced lung vascular permeability and acute lung injury in mice after 18hr. Our results suggest that mexenone-induced endothelial cell (EC) barrier stabilization could be effective in treating sepsis patients.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acute Lung Injury / chemically induced
  • Acute Lung Injury / drug therapy
  • Acute Lung Injury / metabolism
  • Acute Lung Injury / pathology
  • Acute Lung Injury / prevention & control
  • Animals
  • Antigens, CD / metabolism
  • Cadherins / metabolism
  • Capillary Permeability / drug effects
  • Cattle
  • Endothelial Cells* / drug effects
  • Endothelial Cells* / metabolism
  • Lipopolysaccharides*
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Sepsis* / chemically induced
  • Sepsis* / drug therapy
  • Sepsis* / metabolism

Substances

  • Lipopolysaccharides
  • Cadherins
  • Antigens, CD
  • cadherin 5

Grants and funding

This research was supported by the Basic Science Research Program awarded to SY through the National Research Foundation of Korea (NRF) funded by the Ministry of Education (202103890002). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.