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Updated: Feb 8, 2026

Isolation of Human Umbilical Vein Endothelial Cells HUVEC
Published on: April 28, 2007
Anti-Inflammatory Effects of Taraxasterol on LPS-Stimulated Human Umbilical Vein Endothelial Cells
Feng Zheng1, Xiaomeng Dong2, Xiangzhu Meng2
1Department of Infectious Disease, Qilu Hospital of Shandong University, Jinan, 250012, Shandong Province, China. zhengfeng1812@sina.com.
In the present study, we used the human umbilical vein endothelial cells (HUVECs) to investigate the anti-inflammatory effects and mechanism of taraxasterol on vascular inflammation. HUVECs were pre-treated with taraxasterol 1 h before lipopolysaccharide (LPS) treatment. The concentrations of TNF-α, IL-8, PGE2, and NO were measured. The expression of VCAM-1, ICAM-1, iNOS, COX-2, NF-κB, and LXRα was detected by western blot analysis. The results showed that taraxasterol not only reduced the production of TNF-α, IL-8, PGE2, and NO induced by LPS, but also reduced the expression of iNOS and COX-2. Taraxasterol also suppressed LPS-induced NF-κB activation and VCAM-1 and ICAM-1 expression. Furthermore, taraxasterol concentration-dependently increased the expression of LXRα. The inhibition of taraxasterol on TNF-α, IL-8, PGE2, and NO production can be reversed by geranylgeranyl diphosphate (GGPP, the LXRα inhibitor). Here, we found that taraxasterol inhibited vascular inflammation through activating LXRα.
In the present study, we used the human umbilical vein endothelial cells (HUVECs) to investigate the anti-inflammatory effects and mechanism of taraxasterol on vascular inflammation. HUVECs were pre-treated with taraxasterol 1 h before lipopolysaccharide (LPS) treatment. The concentrations of TNF-α, IL-8, PGE2, and NO were measured. The expression of VCAM-1, ICAM-1, iNOS, COX-2, NF-κB, and LXRα was detected by western blot analysis. The results showed that taraxasterol not only reduced the production of TNF-α, IL-8, PGE2, and NO induced by LPS, but also reduced the expression of iNOS and COX-2. Taraxasterol also suppressed LPS-induced NF-κB activation and VCAM-1 and ICAM-1 expression. Furthermore, taraxasterol concentration-dependently increased the expression of LXRα. The inhibition of taraxasterol on TNF-α, IL-8, PGE2, and NO production can be reversed by geranylgeranyl diphosphate (GGPP, the LXRα inhibitor). Here, we found that taraxasterol inhibited vascular inflammation through activating LXRα.
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