Docosahexaenoic Acid Selectively Attenuates Induction of Vascular Cell Adhesion Molecule–1 and Subsequent Monocytic Cell Adhesion to Human Endothelial Cells Stimulated by Tumor Necrosis Factor–α
Authors
Discussion
Loading...
Member takes
Implication
In vitro study reveals docosahexaenoic acid reduces TNF-α-induced VCAM-1 expression and monocyte adhesion in human endothelial cells, highlighting a mechanism for vascular protection.
Key Points
- To investigate whether docosahexaenoic acid alters cytokine-induced adhesion molecule expression and leukocyte attachment in endothelial cells, and to characterize the mediating signaling pathways.
- Incorporated docosahexaenoic acid (DHA), eicosapentaenoic acid (EPA), or arachidonic acid into human umbilical vein endothelial cell (HUVEC) phospholipids before stimulation with TNF-alpha, interleukin-1 beta, or interferon gamma.
- Quantified endothelial surface expression of VCAM-1, ICAM-1, and ELAM-1, along with U937 monocytic cell adhesion and VCAM-1 mRNA transcription.
- Assessed nuclear factor-kappa B activation via gel-shift analysis and measured phosphatidylcholine-specific phospholipase C (PC-PLC) activity via [14C]diacylglycerol synthesis using PC-PLC inhibitor D609.
- DHA dose-dependently reduced TNF-alpha-induced VCAM-1 surface expression, mRNA levels, and monocytic cell adhesion without altering ICAM-1, ELAM-1, or interleukin-1 beta-induced VCAM-1 expression.
- Neither eicosapentaenoic acid nor arachidonic acid altered TNF-alpha-stimulated VCAM-1 expression or PC-PLC activity, whereas DHA treatment produced a fourfold enrichment in phosphatidylcholine.
- DHA and the PC-PLC inhibitor D609 each suppressed TNF-alpha-induced PC-PLC activation and inhibited nuclear factor-kappa B mobilization, whereas exogenous 1,2-diacylglycerol stimulated VCAM-1 expression.
Cite This Study
Weber et al. (1995) studied this question.