Anti-Inflammatory Effect of the Natural H2S-Donor Erucin in Vascular Endothelium

Int J Mol Sci. 2022 Dec 9;23(24):15593. doi: 10.3390/ijms232415593.


Vascular inflammation (VI) represents a pathological condition that progressively affects the integrity and functionality of the vascular wall, thus leading to endothelial dysfunction and the onset of several cardiovascular diseases. Therefore, the research of novel compounds able to prevent VI represents a compelling need. In this study, we tested erucin, the natural isothiocyanate H2S-donor derived from Eruca sativa Mill. (Brassicaceae), in an in vivo mouse model of lipopolysaccharide (LPS)-induced peritonitis, where it significantly reduced the amount of emigrated CD11b positive neutrophils. We then evaluated the anti-inflammatory effects of erucin in LPS-challenged human umbilical vein endothelial cells (HUVECs). The pre-incubation of erucin, before LPS treatment (1, 6, 24 h), significantly preserved cell viability and prevented the increase of reactive oxygen species (ROS) and tumor necrosis factor alpha (TNF-α) levels. Moreover, erucin downregulated endothelial hyperpermeability and reduced the loss of vascular endothelial (VE)-Cadherin levels. In addition, erucin decreased vascular cell adhesion molecule 1 (VCAM-1), cyclooxygenase-2 (COX-2) and microsomal prostaglandin E-synthase 1 (mPGES-1) expression. Of note, erucin induced eNOS phosphorylation and counteracted LPS-mediated NF-κB nuclear translocation, an effect that was partially abolished in the presence of the eNOS inhibitor L-NAME. Therefore, erucin can control endothelial function through biochemical and genomic positive effects against VI.

Keywords: Eruca sativa Mill.; endothelial dysfunction; erucin; hydrogen sulfide; isothiocyanates; vascular inflammation.

MeSH terms

  • Animals
  • Anti-Inflammatory Agents / metabolism
  • Anti-Inflammatory Agents / pharmacology
  • Endothelium, Vascular* / metabolism
  • Human Umbilical Vein Endothelial Cells / metabolism
  • Humans
  • Lipopolysaccharides / pharmacology
  • Mice
  • NF-kappa B / metabolism
  • Signal Transduction*
  • Tumor Necrosis Factor-alpha / metabolism
  • Vascular Cell Adhesion Molecule-1 / metabolism


  • erucin
  • Lipopolysaccharides
  • NF-kappa B
  • Vascular Cell Adhesion Molecule-1
  • Tumor Necrosis Factor-alpha
  • Anti-Inflammatory Agents