The effect of endothelial cells’ exposure to dibutyl phthalate (DBP) on monocyte adhesion is largely unknown. We evaluated monocyte adhesion to DBP-exposed endothelial cells by combining three approaches: short-term exposure (24 h) of EA.hy926 cells to 10, 10, and 10 M DBP, long-term exposure (12 weeks) of EA.hy926 cells to 10, 10, and 10 M DBP, and exposure of rats (28 and 90 days) to 100, 500, and 5000 mg DBP/kg food. Monocyte adhesion to human EA.hy926 and rat aortic endothelial cells, expression of selected cellular adhesion molecules and chemokines, and the involvement of extracellular signal-regulated kinase 1/2 (ERK1/2) were analyzed. We observed increased monocyte adhesion to DBP-exposed EA.hy926 cells and to rat aortic endothelium . ERK1/2 inhibitor prevented monocyte adhesion to DBP-exposed EA.hy926 cells in short-term exposure experiments. Increased ERK1/2 phosphorylation in rat aortic endothelium and transient decrease in ERK1/2 activation following long-term exposure of EA.hy926 cells to DBP were also observed. In summary, exposure of endothelial cells to DBP promotes monocyte adhesion, thus suggesting a possible role for this phthalate in the development of atherosclerosis. ERK1/2 signaling could be the mediator of monocyte adhesion to DBP-exposed endothelial cells, but only after short-term high-level exposure.

中文翻译：

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内皮细胞在体外和体内暴露于邻苯二甲酸二丁酯可促进单核细胞粘附

内皮细胞暴露于邻苯二甲酸二丁酯 (DBP) 对单核细胞粘附的影响目前尚不清楚。我们通过结合三种方法评估单核细胞对暴露于 DBP 的内皮细胞的粘附：EA.hy926 细胞短期暴露于 10、10 和 10 M DBP，EA.hy926 长期暴露（12 周）细胞暴露于 10、10 和 10 M DBP，以及大鼠（28 和 90 天）暴露于 100、500 和 5000 mg DBP/kg 食物。分析了单核细胞对人 EA.hy926 和大鼠主动脉内皮细胞的粘附、选定细胞粘附分子和趋化因子的表达以及细胞外信号调节激酶 1/2 (ERK1/2) 的参与。我们观察到单核细胞对暴露于 DBP 的 EA.hy926 细胞和大鼠主动脉内皮的粘附增加。在短期暴露实验中，ERK1/2 抑制剂可防止单核细胞粘附到 DBP 暴露的 EA.hy926 细胞上。还观察到 EA.hy926 细胞长期暴露于 DBP 后，大鼠主动脉内皮中 ERK1/2 磷酸化增加，ERK1/2 激活短暂减少。总之，内皮细胞暴露于 DBP 会促进单核细胞粘附，因此表明邻苯二甲酸盐在动脉粥样硬化的发展中可能发挥作用。 ERK1/2 信号传导可能是单核细胞粘附到暴露于 DBP 的内皮细胞的介质，但仅限于短期高水平暴露后。