Loading…

Curcumin Protects against Atherosclerosis in Apolipoprotein E‑Knockout Mice by Inhibiting Toll-like Receptor 4 Expression

Toll-like receptor 4 (TLR4) has been reported to play a critical role in the pathogenesis of atherosclerosis, the current study aimed to investigate whether curcumin suppresses atherosclerosis development in ApoE-knockout (ApoE–/–) mice by inhibiting TLR4 expression. ApoE–/– mice were fed a high-fat...

Full description

Saved in:
Bibliographic Details
Published in:Journal of agricultural and food chemistry 2018-01, Vol.66 (2), p.449-456
Main Authors: Zhang, Shanshan, Zou, Jun, Li, Peiyang, Zheng, Xiumei, Feng, Dan
Format: Article
Language:English
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Toll-like receptor 4 (TLR4) has been reported to play a critical role in the pathogenesis of atherosclerosis, the current study aimed to investigate whether curcumin suppresses atherosclerosis development in ApoE-knockout (ApoE–/–) mice by inhibiting TLR4 expression. ApoE–/– mice were fed a high-fat diet supplemented with or without curcumin (0.1% w/w) for 16 weeks. Curcumin supplementation significantly reduced TLR4 expression and macrophage infiltration in atherosclerotic plaques. Curcumin also reduced aortic interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1) expression, nuclear factor-κB (NF-κB) activity, and plasma IL-1β, TNF-α, soluble VCAM-1 and ICAM-1 levels. In addition, aortic sinus sections revealed that curcumin treatment reduced the extent of atherosclerotic lesions and inhibited atherosclerosis development. In vitro, curcumin inhibited NF-κB activation in macrophages and reduced TLR4 expression induced by lipopolysaccharide. Our results indicate that curcumin protects against atherosclerosis at least partially by inhibiting TLR4 expression and its related inflammatory reaction.
ISSN:0021-8561
1520-5118
DOI:10.1021/acs.jafc.7b04260