血管炎症(VI)代表逐渐影响血管壁的完整性和功能的病理状况。从而导致内皮功能障碍和几种心血管疾病的发作。因此,能够预防VI的新型化合物的研究代表了迫切的需要。在这项研究中,我们测试了芥酸,来自芥菜的天然异硫氰酸酯H2S供体。(十字花科),在脂多糖(LPS)诱导的腹膜炎的体内小鼠模型中,显着减少了CD11b阳性中性粒细胞的数量。然后,我们评估了芥酸素在LPS攻击的人脐静脉内皮细胞(HUVEC)中的抗炎作用。芥酸素的预孵化,LPS治疗前(1、6、24小时),显着保持细胞活力,并防止活性氧(ROS)和肿瘤坏死因子α(TNF-α)水平的增加。此外,芥酸素下调内皮高通透性并降低血管内皮(VE)-钙黏着蛋白水平的损失。此外,芥酸素降低血管细胞粘附分子1(VCAM-1),环氧合酶-2(COX-2)和微粒体前列腺素E-合酶1(mPGES-1)表达。值得注意的是,芥酸诱导的eNOS磷酸化和抑制LPS介导的NF-κB核转位,在存在eNOS抑制剂L-NAME的情况下部分消除的效应。因此,芥酸素可以通过对VI的生化和基因组阳性作用来控制内皮功能。
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.