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.