Notoginsenoside Fc alleviates oxidized low-density lipoprotein-induced endothelial cell dysfunction and upregulates PPAR-γ in vitro.

Abstract

Deep venous thrombosis (DVT) is a prevalent vascular disease and a major cause of morbidity and mortality worldwide. Notoginsenoside Fc (NFc) is a protopanaxadiol-type saponin that has been shown to have beneficial effects on several disorders. However, its function in DVT is unclear. Human umbilical vein endothelial cells (HUVECs) were treated with oxidized low-density lipoprotein (ox-LDL) to mimic DVT in vitro and treated with NFc to investigate its functions. CCK-8 assay was utilized for measuring cell viability. Western blotting was used for detecting protein levels of proinflammatory cytokines, apoptosis-related markers, and peroxisome proliferator-activated receptor-γ (PPAR-γ). Flow cytometry was performed for cell apoptosis detection. Levels of oxidative stress-related markers were examined by the DCFH-DA method and ELISA. RT-qPCR was utilized for the measurement of PPAR-γ mRNA level. NFc increased the viability and suppressed inflammation, apoptosis, and oxidative stress in ox-LDL-treated HUVECs. NFc treatment induced upregulation of PPAR-γ in HUVECs. NFc mitigates ox-LDL-induced dysfunction of HUVECs.