4.7 Article

The H2S-Donor Erucin Exhibits Protective Effects against Vascular Inflammation in Human Endothelial and Smooth Muscle Cells

期刊

ANTIOXIDANTS
卷 10, 期 6, 页码 -

出版社

MDPI
DOI: 10.3390/antiox10060961

关键词

vascular inflammation; endothelial permeability; H2S-donor; erucin; isothiocyanate; Eruca sativa Mill; vascular wall; hydrogen sulfide

资金

  1. Bando per il finanziamento di Dimostratori Tecnologici DT (DT grant) by University of Pisa, MIUR, Italy
  2. CREA Council for Agricultural Research and Economics, Italy
  3. Italian Ministry of Instruction, University and Research (MIUR), PON Ricerca e Innovazione 2014-2020-Azione II, by the COMETA research project [ARS01_00606, 1741, CUP B26G18000200004-COR 545910]
  4. Italian Ministry of University and Research (MIUR) [PRIN 2017XP72RF]

向作者/读者索取更多资源

The study demonstrates that erucin can effectively prevent high glucose-induced endothelial dysfunction and inflammation by inhibiting ROS and inflammatory markers levels, protecting vascular cell integrity, and also has a certain inhibitory effect on the increase in vascular permeability.
Preservation of vascular wall integrity against degenerative processes associated with ageing, fat-rich diet and metabolic diseases is a timely therapeutical challenge. The loss of endothelial function and integrity leads to cardiovascular diseases and multiorgan inflammation. The protective effects of the H2S-donor erucin, an isothiocyanate purified by Eruca sativa Mill. seeds, were evaluated on human endothelial and vascular smooth muscle cells. In particular, erucin actions were evaluated on cell viability, ROS, caspase 3/7, inflammatory markers levels and the endothelial hyperpermeability in an inflammatory model associated with high glucose concentrations (25 mM, HG). Erucin significantly prevented the HG-induced decrease in cell viability as well as the increase in ROS, caspase 3/7 activation, and TNF-alpha and IL-6 levels. Similarly, erucin suppressed COX-2 and NF-kappa B upregulation associated with HG exposure. Erucin also caused a significant inhibition of p22phox subunit expression in endothelial cells. In addition, erucin significantly prevented the HG-induced increase in endothelial permeability as also confirmed by the quantification of the specific markers VE-Cadherin and ZO-1. In conclusion, our results assess anti-inflammatory and antioxidant effects by erucin in vascular cells undergoing HG-induced inflammation and this protection parallels the preservation of endothelial barrier properties.

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