PDF(Pubmed)
Abstract：
UNASSIGNED: The maintenance of endothelial barrier function is essential for vasal homeostasis and prevention of cardiovascular diseases. Among the toxic stimuli involved in the initiation of atherosclerotic lesions, Gram negative lipopolysaccharide (LPS) has been reported to be able to trigger endothelial dysfunction, through the alteration of barrier permeability and inflammatory response. Hydroxytyrosol (HT) and tyrosol (Tyr), the major phenolic compounds of extra virgin olive oil (EVOO), as wells as their circulating sulphated and glucuronidated metabolites have been shown to exert anti-inflammatory effects at endothelial level.
UNASSIGNED: In this study we investigated the protective effects of HT and Tyr metabolites on LPS-induced alteration of permeability in Human Umbilical Vein Endothelial Cells (HUVEC) monolayers and examined underlying signaling pathways, focusing on tight junction (TJ) proteins, mitogen-activated protein kinase (MAPK) and NOD-, LRR-and pyrin domain-containing protein 3 (NLRP3) inflammasome activation.
UNASSIGNED: It was shown that LPS-increased permeability in HUVEC cells was due to the alteration of TJ protein level, following the activation of MAPK and NLRP3. HT and Tyr sulphated and glucuronidated metabolites were able to limit the effects exerted by LPS, acting as signaling molecules with an efficacy comparable to that of their precursors HT and Tyr.
UNASSIGNED: The obtained results add a further piece to the understanding of HT and Tyr metabolites mechanisms of action in vascular protection.
UNASSIGNED: In this study we investigated the protective effects of HT and Tyr metabolites on LPS-induced alteration of permeability in Human Umbilical Vein Endothelial Cells (HUVEC) monolayers and examined underlying signaling pathways, focusing on tight junction (TJ) proteins, mitogen-activated protein kinase (MAPK) and NOD-, LRR-and pyrin domain-containing protein 3 (NLRP3) inflammasome activation.
UNASSIGNED: It was shown that LPS-increased permeability in HUVEC cells was due to the alteration of TJ protein level, following the activation of MAPK and NLRP3. HT and Tyr sulphated and glucuronidated metabolites were able to limit the effects exerted by LPS, acting as signaling molecules with an efficacy comparable to that of their precursors HT and Tyr.
UNASSIGNED: The obtained results add a further piece to the understanding of HT and Tyr metabolites mechanisms of action in vascular protection.
摘要：
■维持内皮屏障功能对于血管稳态和预防心血管疾病至关重要。在动脉粥样硬化病变开始的毒性刺激中，据报道，革兰氏阴性脂多糖（LPS）能够引发内皮功能障碍，通过屏障通透性和炎症反应的改变。羟基酪醇（HT）和酪醇（Tyr），特级初榨橄榄油（EVOO）的主要酚类化合物，以及它们的循环硫酸化和葡萄糖醛酸化代谢物已被证明在内皮水平上发挥抗炎作用。
■在这项研究中，我们研究了HT和Tyr代谢物对LPS诱导的人脐静脉内皮细胞（HUVEC）单层通透性改变的保护作用，并检查了潜在的信号通路。专注于紧密连接（TJ）蛋白，丝裂原活化蛋白激酶（MAPK）和NOD-，含有LRR和pyrin结构域的蛋白3（NLRP3）炎性体激活。
■研究表明，HUVEC细胞中LPS增加的通透性是由于TJ蛋白水平的改变，MAPK和NLRP3激活后。HT和Tyr硫酸化和葡萄糖醛酸化代谢产物能够限制LPS的作用，充当信号分子，其功效与其前体HT和Tyr相当。
■获得的结果为了解HT和Tyr代谢物在血管保护中的作用机制提供了进一步的依据。
■在这项研究中，我们研究了HT和Tyr代谢物对LPS诱导的人脐静脉内皮细胞（HUVEC）单层通透性改变的保护作用，并检查了潜在的信号通路。专注于紧密连接（TJ）蛋白，丝裂原活化蛋白激酶（MAPK）和NOD-，含有LRR和pyrin结构域的蛋白3（NLRP3）炎性体激活。
■研究表明，HUVEC细胞中LPS增加的通透性是由于TJ蛋白水平的改变，MAPK和NLRP3激活后。HT和Tyr硫酸化和葡萄糖醛酸化代谢产物能够限制LPS的作用，充当信号分子，其功效与其前体HT和Tyr相当。
■获得的结果为了解HT和Tyr代谢物在血管保护中的作用机制提供了进一步的依据。
