Astragalus polysaccharides suppress ICAM-1 and VCAM-1 expression in TNF-α-treated human vascular endothelial cells by blocking NF-κB activation

Abstract

Aim: To investigate the effects of Astragalus polysaccharides (APS) on tumor necrosis factor (TNF)-α-induced inflammatory reactions in human umbilical vein endothelial cells (HUVECs) and to elucidate the underlying mechanisms. Methods: HUVECs were treated with TNF-α for 24 h. The amounts of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) were determined with Western blotting. HUVEC viability and apoptosis were detected using cell viability assay and Hoechst staining, respectively. Reactive oxygen species (ROS) production was measured by DHE staining. Monocyte and HUVEC adhesion assay was used to detect endothelial cell adhesive function. NF-κB activation was detected with immunofluorescence. Results: TNF-α (1-80 ng/mL) caused dose-and time-dependent increases of ICAM-1 and VCAM-1 expression in HUVECs, accompanied by significant augmentation of IκB phosphorylation and NF-κB translocation into the nuclei. Pretreatment with APS (10 and 50 µg/mL) significantly attenuated TNFα-induced upregulation of ICAM-1, VCAM-1, and NF-κB translocation. Moreover, APS significantly reduced apoptosis, ROS generation and adhesion function damage in TNF-α-treated HUVECs. Conclusion: APS suppresses TNFα-induced adhesion molecule expression by blocking NF-κB signaling and inhibiting ROS generation in HUVECs. The results suggest that APS may be used to treat and prevent endothelial cell injury-related diseases.

Lipopolysaccharide induces ICAM-1 expression via a c-Src/NADPH oxidase/ROS-dependent NF-κB pathway in human pulmonary alveolar epithelial cells

“…Several lines of evidence have demonstrated that ROS contribute to ICAM-1 expression induced by different stimuli in various cell types (8,34). In addition, NADPH oxidase is an important enzymatic source for the production of ROS under various pathologic conditions.…”

β-elemene inhibits monocyte–endothelial cells interactions via reactive oxygen species/MAPK/NF-κB signaling pathway in vitro

“…Accumulated evidence demonstrates that monocyte infiltration plays a crucial role in the pathophysiology of coronary artery diseases including atherosclerosis, which can not only initiate and propagate the accumulation of monocyte-derived macrophages but also produce inflammatory mediators that destabilize atherosclerotic plaques (Kartikasari et al, 2009;Zhu et al, 2013). The monocyte-endothelium cells interactions consist of consecutive processes of monocytes adhesion 3 / 29 and infiltration through the endothelium.…”

Lauric acid abolishes interferon-gamma (IFN-γ)-induction of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) expression in human macrophages

“…Lauric acid has been shown to reduce the expression of transcription factor, NF-kB [21] . NF-kB is a pro-inflammatory transcription factor that activates immune and inflammatory response by controlling the genes expression of a wide spectrum of inflammatory cytokines and cell adhesion molecules [22][23][24] . Hence, the reduction of IFN-g induced VCAM-1 and ICAM-1 expression might be caused by the diminished cellular NF-kB concentration after the treatment of lauric acid.…”