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Inhibitory Effect of an Urotensin II Receptor Antagonist on Proinflammatory Activation Induced by Urotensin II in Human Vascular Endothelial Cells

机译:血管紧张素Ⅱ受体拮抗剂对血管紧张素Ⅱ诱导的人血管内皮细胞促炎性激活的抑制作用

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摘要

In this study, we investigated the effects of a selective urotensin II (UII) receptor antagonist, SB-657510, on the inflammatory response induced by UII in human umbilical vein endothelial cells (EA.hy926) and human monocytes (U937). UII induced inflammatory activation of endothelial cells through expression of proinflammatory cytokines (IL-1β and IL-6), adhesion molecules (VCAM-1), and tissue factor (TF), which facilitates the adhesion of monocytes to EA.hy926 cells. Treatment with SB-657510 significantly inhibited UII-induced expression of IL-1β, IL-6, and VCAM-1 in EA.hy926 cells. Further, SB-657510 dramatically blocked the UII-induced increase in adhesion between U937 and EA.hy926 cells. In addition, SB-657510 remarkably reduced UII-induced expression of TF in EA.hy926 cells. Taken together, our results demonstrate that the UII antagonist SB-657510 decreases the progression of inflammation induced by UII in endothelial cells.
机译:在这项研究中,我们研究了选择性尿素II(UII)受体拮抗剂SB-657510对UII在人脐静脉内皮细胞(EA.hy926)和人单核细胞(U937)中诱导的炎症反应的影响。 UII通过促炎性细胞因子(IL-1β和IL-6),黏附分子(VCAM-1)和组织因子(TF)的表达诱导内皮细胞的炎性活化,从而促进单核细胞与EA.hy926细胞的黏附。 SB-657510处理可显着抑制EA.hy926细胞中UII诱导的IL-1β,IL-6和VCAM-1表达。此外,SB-657510显着阻断了UII诱导的U937与EA.hy926细胞之间粘附的增加。另外,SB-657510显着降低了EA.hy926细胞中UII诱导的TF表达。两者合计,我们的结果表明,UII拮抗剂SB-657510减少了UII在内皮细胞中诱导的炎症进程。

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