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Updated: Feb 26, 2026
On-Chip Endothelial Inflammatory Phenotyping
Published on: July 21, 2012
Curcumin modulates endothelial permeability and monocyte transendothelial migration by affecting endothelial cell
Laurent-Emmanuel Monfoulet1, Sylvie Mercier1, Dominique Bayle1
1Université Clermont Auvergne, INRA, UNH, CRNH Auvergne, F-63000 Clermont-Ferrand, France.
Insights
Curcumin, a compound found in turmeric, reduces immune cell movement across blood vessel walls. This study shows curcumin improves endothelial barrier function and may prevent atherosclerosis by regulating cell dynamics and inhibiting inflammatory pathways.
Area of Science:
- Cardiovascular Biology
- Immunology
- Pharmacology
Background:
- Curcumin exhibits beneficial properties for cardiometabolic health.
- Previous studies demonstrated curcumin's ability to reduce immune cell infiltration and prevent atherosclerosis in mice.
- Understanding curcumin's effects on endothelial cells and inflammatory pathways is crucial for its therapeutic application.
Purpose of the Study:
- To investigate the effect of curcumin on monocyte adhesion and transendothelial migration (TEM).
- To elucidate the underlying molecular mechanisms by which curcumin influences endothelial cell function.
- To assess curcumin's impact on endothelial permeability and cell morphology under static and shear stress conditions.
Main Methods:
- Human umbilical vein endothelial cells (HUVECs) were pre-exposed to curcumin before TNF-α activation.
- Monocyte adhesion, TEM, and endothelial permeability assays were performed under static and shear stress.
- Gene expression analysis using macroarrays and molecular docking were employed to study signaling pathways.
Main Results:
- Curcumin significantly reduced monocyte adhesion and TEM under both static and shear stress conditions.
- Curcumin prevented TNF-α-induced changes in endothelial permeability and HUVEC area.
- Curcumin modulated 15 genes involved in cytoskeleton and endothelial junction dynamics, and inhibited NF-κB signaling.
Conclusions:
- Curcumin effectively reduces monocyte transendothelial migration via multimodal regulation of endothelial cell dynamics.
- Curcumin enhances vascular endothelial barrier function, suggesting potential benefits for preventing inflammatory vascular diseases.
- The findings support curcumin's therapeutic potential in managing cardiometabolic and inflammatory vascular conditions.
Abstract:
Curcumin is a phenolic compound that exhibits beneficial properties for cardiometabolic health. We previously showed that curcumin reduced the infiltration of immune cells into the vascular wall and prevented atherosclerosis development in mice. This study aimed to investigate the effect of curcumin on monocyte adhesion and transendothelial migration (TEM) and to decipher the underlying mechanisms of these actions. Human umbilical vein endothelial cells (HUVECs) were exposed to curcumin (0.5-1μM) for 3h prior to their activation by Tumor Necrosis Factor alpha (TNF-α). Endothelial permeability, monocyte adhesion and transendothelial migration assays were conducted under static condition and shear stress that mimics blood flow. We further investigated the impact of curcumin on signaling pathways and on the expression of genes using macroarrays. Pre-exposure of endothelial cells to curcumin reduced monocyte adhesion and their transendothelial migration in both static and shear stress conditions. Curcumin also prevented changes in both endothelial permeability and the area of HUVECs when induced by TNF-α. We showed that curcumin modulated the expression of 15 genes involved in the control of cytoskeleton and endothelial junction dynamic. Finally, we showed that curcumin inhibited NF-κB signaling likely through an antagonist interplay with several kinases as suggested by molecular docking analysis. Our findings demonstrate the ability of curcumin to reduce monocyte TEM through a multimodal regulation of the endothelial cell dynamics with a potential benefit on the vascular endothelial function barrier.
