Department of Clinical Pharmacy, School of Pharmacy, Shandong University, Jinan, Shandong 250012, P.R. China.
Can J Physiol Pharmacol. 2010 May;88(5):576-83. doi: 10.1139/y10-028.
Prostaglandin E1 (PGE1) is a member of the prostaglandins and has a variety of cardiovascular protective effects. Increasing attention has been paid to the anti-inflammation activity of PGE1, but little direct evidence has been found. We investigated the effects of PGE1 on cell adhesion and inflammation and the mechanisms responsible for this activity in tumor necrosis factor (TNF)-treated human umbilical vein endothelial cells. Results demonstrated that pretreatment with PGE1 decreased the adhesion between vascular endothelial cells and monocytes, reduced the expression of vascular cell adhesion molecule-1, intercellular adhesion molecule-1, and E-selectin in vascular endothelial cells. In addition, PGE1 suppressed TNF-induced NF-kappaB activation and production of reactive oxygen species. We concluded that PGE1 suppressed the vascular inflammatory process, which might be closely related to the inhibition of reactive oxygen species and NF-kappaB activation in human umbilical vein endothelial cells.
前列腺素 E1(PGE1)是前列腺素家族的一员,具有多种心血管保护作用。PGE1 的抗炎活性越来越受到关注,但很少有直接证据。我们研究了 PGE1 对肿瘤坏死因子(TNF)处理的人脐静脉内皮细胞黏附与炎症的影响及其作用机制。结果表明,PGE1 预处理可降低血管内皮细胞与单核细胞之间的黏附,减少血管内皮细胞中血管细胞黏附分子-1、细胞间黏附分子-1 和 E-选择素的表达。此外,PGE1 抑制 TNF 诱导的 NF-κB 激活和活性氧的产生。我们的结论是,PGE1 抑制了血管炎症过程,这可能与 PGE1 抑制人脐静脉内皮细胞中活性氧和 NF-κB 激活密切相关。