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Sulforaphane improves endothelial function and reduces placental oxidative stress in vitro

机译:亚磺酸盐改善内皮函数并减少体外胎盘氧化胁迫

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Introduction: The maternal endothelial dysfunction characteristic of preeclampsia arises, in part, from excessive placental production of anti-angiogenic factors, including soluble Flt-1, soluble endoglin and activin A, inducing oxidative stress. We assessed whether the antioxidant and NRF2-activator sulforaphane could mitigate endothelial and trophoblast dysfunction in vitro.Methods: We induced dysfunction in human umbilical vein endothelial cells (HUVECs) with TNF-a, assessing endothelial activation and dysfunction (endothelin-1, vascular cell adhesion molecule; VCAM1, intracellular adhesion molecule; ICAM1, e-selectin and endothelial permeability) in the presence or absence of sulforaphane. We also assessed the effects of sulforaphane in mitigating hypoxic and hyperoxic injury in term placental ex-plants by measuring secretion of anti-angiogenic factors. To assess the role of NRF2 we silenced NRF2 in HUVECs and primary trophoblast cells.
机译:介绍:母体内皮功能障碍的特征在于抗血管生成因子的过度胎盘产生,包括可溶性FLT-1,可溶性内切胶剂A,诱导氧化应激。 我们评估了抗氧化剂和NRF2-活化剂磺橡胶是否可以减轻体外内皮和滋养剂功能障碍。方法:我们用TNF-A诱导人脐静脉内皮细胞(HUVECS)的功能障碍,评估内皮活化和功能障碍(内皮素-1,血管细胞 粘附分子; Vcam1,细胞内粘附分子; ICAM1,E-SELIENIN和内皮渗透率)在存在或不存在的亚磺甲烷中。 我们还通过测量抗血管生成因子的分泌来评估嗜睡在胎儿胎儿术中缺氧和高氧损伤的影响。 评估NRF2的作用我们在Huvecs和初级滋养细胞中静音NRF2。

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