期刊
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
卷 23, 期 24, 页码 -出版社
MDPI
DOI: 10.3390/ijms232415593
关键词
vascular inflammation; endothelial dysfunction; hydrogen sulfide; erucin; isothiocyanates; Eruca sativa Mill
资金
- Bando per il finanziamento di Dimostratori Tecnologici DT (DT grant)
- University of Pisa, MIUR, Italy
- CREA Council for Agricultural Research and Economics, Italy
- Italian Ministry of Instruction, University and Research (MIUR)
- COMETA research project Colture autoctone mediterranee e loro valorizzazione con tecnologie avanzate di chimica verde [ARS01_00606]
- Italian Ministry of Instruction, University and Research (MIUR), PON Ricerca ed Innovazione [1741, CUP B26G18000200004-COR 545910, INBIOMED_ARS01_01081]
- Italian Ministry of University and Research (MIUR) [PRIN 2017XP72RF]
- University of Pisa
- University of Stanford
- Fondazione Umberto Veronesi, Milan (Italy)
This study found that erucin has anti-inflammatory effects, reducing the emigration of neutrophils, protecting endothelial cells from oxidative damage and tumor necrosis factor α-mediated injury, decreasing endothelial hyperpermeability, and reducing the expression of inflammatory proteins. Additionally, erucin regulates endothelial function through inducing eNOS phosphorylation and inhibiting NF-kappa B nuclear translocation.
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-alpha) 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-kappa B 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.
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