Journal
MOLECULES
Volume 21, Issue 2, Pages -Publisher
MDPI
DOI: 10.3390/molecules21020195
Keywords
naringin; atherosclerosis; TNF-alpha; chemokines; NF-kappa B
Funding
- Chang Gung Memorial Hospital [CMRPG5B0101, 891121, 891122, 891123, 8C0291]
Ask authors/readers for more resources
Naringin has been reported to have an anti-atherosclerosis effect but the underlying mechanism is not fully understood. The aim of this study is to investigate the impact of naringin on the TNF--induced expressions of cell adhesion molecules, chemokines and NF-B signaling pathway in human umbilical vein endothelial cells (HUVECs). The experiments revealed that naringin, at concentrations without cytotoxicity, dose-dependently inhibited the adhesion of THP-1 monocytes to the TNF--stimulated HUVECs. The TNF--induced expressions of cell adhesion molecules, including VCAM-1, ICAM-1 and E-selectin, at both the mRNA and protein levels, were significantly suppressed by naringin in a dose dependent manner. In addition, the TNF--induced mRNA and protein levels of chemokines, including fractalkine/CX3CL1, MCP-1 and RANTES, were also reduced by naringin. Naringin significantly inhibited TNF--induced nuclear translocation of NF-B, which resulted from the inhibited phosphorylation of IKK/, IB- and NF-B. Altogether, we proposed that naringin modulated TNF--induced expressions of cell adhesion molecules and chemokines through the inhibition of TNF--induced activation of IKK/NF-B signaling pathway to exert the anti-atherosclerotic effect.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available