Abstract |
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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Authors | Feng Zheng, Xiaomeng Dong, Xiangzhu Meng |
Journal | Inflammation
(Inflammation)
Vol. 41
Issue 5
Pg. 1755-1761
(Oct 2018)
ISSN: 1573-2576 [Electronic] United States |
PMID | 29951871
(Publication Type: Journal Article)
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Chemical References |
- Anti-Inflammatory Agents
- Cytokines
- Lipopolysaccharides
- Liver X Receptors
- NF-kappa B
- Sterols
- Triterpenes
- taraxasterol
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Topics |
- Anti-Inflammatory Agents
(pharmacology, therapeutic use)
- Cells, Cultured
- Cytokines
(drug effects)
- Human Umbilical Vein Endothelial Cells
(drug effects)
- Humans
- Inflammation
(drug therapy)
- Lipopolysaccharides
- Liver X Receptors
- NF-kappa B
(metabolism)
- Sterols
(pharmacology, therapeutic use)
- Triterpenes
(pharmacology, therapeutic use)
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