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

作者：Zhu, Yu-ping; Shen, Tao; Lin, Ya-jun; Chen, Bei-dong; Ruan, Yang; Cao, Yuan; Qiao, Yue; Man, Yong; Wang, Shu; Li, Jian^*

来源：Acta Pharmacologica Sinica, 2013, 34(8): 1036-1042.

DOI：10.1038/aps.2013.46

• Astragalus polysaccharides
• endothelial cell injury
• TNF-alpha
• ICAM-1
• VCAM-1
• NF-kappa B
• apoptosis
• reactive oxygen species
• atherosclerosis

Aim: To investigate the effects of Astragalus polysaccharides (APS) on tumor necrosis factor (TNF)-alpha-induced inflammatory reactions in human umbilical vein endothelial cells (HUVECs) and to elucidate the underlying mechanisms.
Methods: HUVECs were treated with TNF-alpha 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-kappa B activation was detected with immunofluorescence.
Results: TNF-alpha (1-80 ng/mL) caused dose- and time-dependent increases of ICAM-1 and VCAM-1 expression in HUVECs, accompanied by significant augmentation of I kappa B phosphorylation and NF-kappa B translocation into the nuclei. Pretreatment with APS (10 and 50 mu g/mL) significantly attenuated TNF alpha-induced upregulation of ICAM-1, VCAM-1, and NF-kappa B translocation. Moreover, APS significantly reduced apoptosis, ROS generation and adhesion function damage in TNF-alpha-treated HUVECs.
Conclusion: APS suppresses TNF alpha-induced adhesion molecule expression by blocking NF-kappa B signaling and inhibiting ROS generation in HUVECs. The results suggest that APS may be used to treat and prevent endothelial cell injury-related diseases.

• 出版日期2013-8
• 单位北京医院