Transcriptomic Profiling of TNFa-Stimulated Human Umbilical Vein Endothelial Cells (HUVECs) With and Without Isoginkgetin (ISOGK) Pretreatment.

We demonstrate that ISOGK attenuates endothelial inflammation through mechanistically distinct suppression of NF-?B p65 phosphorylation and nuclear translocation, highlighting its potential as a therapeutic agent for atherosclerosis intervention. This anti-inflammatory effect was associated with significant modulation of inflammatory pathway activation in vascular endothelial cells. Overall design: HUVECs were pretreated with 7.5 µM ISOGK for 12 hours prior to 6-hour stimulation with 10 ng/mL TNFa. Comparative transcriptomic analysis was subsequently performed to characterize ISOGK-mediated modulation of inflammatory responses.

本研究证实，ISOGK可通过以独特分子机制抑制核因子κB p65（NF-κB p65）的磷酸化与核转位，从而减轻内皮炎症，凸显其作为动脉粥样硬化干预治疗剂的应用潜力。该抗炎效应与血管内皮细胞中炎症通路激活的显著调控密切相关。总体实验设计：将人脐静脉内皮细胞（HUVECs）以7.5 μM ISOGK预处理12小时，随后以10 ng/mL 肿瘤坏死因子α（TNF-α）刺激6小时。随后开展比较转录组学分析，以表征ISOGK介导的炎症反应调控特征。