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Purpose <p>In this study we investigated how anthocyanins and their metabolites exert protection on the vasculature by reducing the inflammation-induced monocyte adhesion to endothelial cells, a fundamental stage in endothelial dysfunction (ED) and inflammation.</p> Methods <p>Human umbilical vein endothelial cells (HUVECs) were pre-treated with varying concentrations (1,5 and 10 µM) of cyanidin-3-glucoside or phenolic metabolites, protocatechuic acid (PCA) and vanillic acid (VA), for 24&#xa0;h, followed by TNF-α stimulation for 24&#xa0;h, with or without the presence of THP-1 monocytes for 1&#xa0;h.</p> Results <p>For the co-culture model, the adhesion of fluorescent monocytes attached to HUVECs was quantified, as well as pro-inflammatory cytokine IL-6 and MCP-1 in cell supernatant. Expression levels of transcription factors Nrf2 and NF-κB-p65, as well as vascular cell adhesion molecule-1 (VCAM-1), intracellular cell adhesion molecule (ICAM-1) and heme oxygenase 1 (HO-1) were measured in HUVECs. All treatments prevented the adhesion of monocytes to endothelial cells, which was associated with reductions in IL-6 and MCP-1. Additionally, phenolic metabolites suppressed adhesion molecules, potentially by their ability to upregulate Nrf2 expression and suppress NF-κB p65 phosphorylation. Furthermore, VA caused an upregulation of HO-1 expression.</p> Conclusions <p>Our findings suggest that pre-exposed physiologically relevant concentrations of phenolic metabolites may hinder ED and inflammation by reducing the adhesion of monocytes to endothelial cells and the inflammatory response via the modulation of NF-κB and Nrf2 pathway.</p>

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Cyanidin-3-glucoside phenolic metabolites, protocatechuic acid and vanillic acid, attenuate the adhesion of monocytes to endothelial cells in response to TNF-α by targeting NF-κB and Nrf2 pathways

  • 期刊论文

  • 发表日期：

    2025年6月7日

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  • Joseph Festa,
  • Aamir Hussain,
  • Harprit Singh,
  • Mariasole Da Boit

摘要

Purpose

In this study we investigated how anthocyanins and their metabolites exert protection on the vasculature by reducing the inflammation-induced monocyte adhesion to endothelial cells, a fundamental stage in endothelial dysfunction (ED) and inflammation.

Methods

Human umbilical vein endothelial cells (HUVECs) were pre-treated with varying concentrations (1,5 and 10 µM) of cyanidin-3-glucoside or phenolic metabolites, protocatechuic acid (PCA) and vanillic acid (VA), for 24 h, followed by TNF-α stimulation for 24 h, with or without the presence of THP-1 monocytes for 1 h.

Results

For the co-culture model, the adhesion of fluorescent monocytes attached to HUVECs was quantified, as well as pro-inflammatory cytokine IL-6 and MCP-1 in cell supernatant. Expression levels of transcription factors Nrf2 and NF-κB-p65, as well as vascular cell adhesion molecule-1 (VCAM-1), intracellular cell adhesion molecule (ICAM-1) and heme oxygenase 1 (HO-1) were measured in HUVECs. All treatments prevented the adhesion of monocytes to endothelial cells, which was associated with reductions in IL-6 and MCP-1. Additionally, phenolic metabolites suppressed adhesion molecules, potentially by their ability to upregulate Nrf2 expression and suppress NF-κB p65 phosphorylation. Furthermore, VA caused an upregulation of HO-1 expression.

Conclusions

Our findings suggest that pre-exposed physiologically relevant concentrations of phenolic metabolites may hinder ED and inflammation by reducing the adhesion of monocytes to endothelial cells and the inflammatory response via the modulation of NF-κB and Nrf2 pathway.