PDF(Pubmed)
Abstract：
GHRH regulates the secretion of GH from the anterior pituitary gland, previously associated with cancer progression and inflammation. An emerging body of evidence suggests that GHRHAnt support endothelial barrier function, but the mechanisms mediating these events are not completely understood. In the present study, it is demonstrated that the GHRHAnt JV-1-36 counteracts barrier dysfunction due to LPS or LTA treatment in HUVECs, utilizing the Dextran-FITC assay. Moreover, it is shown in BPAECs that these bacterial toxins increase ROS generation, and that this effect is counteracted by JV-1-36, which reinstates the redox balance. The possible involvement of NEK2 in the beneficial activities of GHRHAnt in IFN-γ- and LPS-triggered hyperpermeability was also assessed, since that kinase is involved in inflammatory responses. NEK2 was increased in the inflamed cells, and JV-1-36 counteracted those endothelial events. Our data support the beneficial effects of GHRHAnt in toxin-induced endothelial injury.
摘要：
GHRH调节垂体前叶GH的分泌，以前与癌症进展和炎症有关。一个新兴的证据表明GHRHAnt支持内皮屏障功能，但是调解这些事件的机制还没有完全理解。在本研究中,已证明GHRHAntJV-1-36可抵消HUVECs中由于LPS或LTA治疗引起的屏障功能障碍，利用葡聚糖-FITC测定。此外，在BPAECs中显示，这些细菌毒素会增加ROS的产生，JV-1-36抵消了这种影响，它恢复了氧化还原平衡。还评估了NEK2可能参与IFN-γ和LPS引发的高通透性中GHRHAnt的有益活性，因为该激酶参与炎症反应。NEK2在发炎的细胞中增加，和JV-1-36抵消了这些内皮事件。我们的数据支持GHRHAnt在毒素诱导的内皮损伤中的有益作用。
