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<p>Natural phenolic acid compounds have been extensively studied for their anti-inflammatory properties, particularly in the context of inflammation-associated diseases. In this study, we investigated the anti-inflammatory effects of <i>trans</i>-cinnamic acid on neutrophil accumulation during inflammatory processes using both in vivo and in vitro approaches. For the in vivo experiments, LPS-induced pleurisy was used in mice pretreated with <i>trans</i>-cinnamic acid. Inflammatory parameters, including plasma leakage, leukocyte infiltration, and proinflammatory cytokine levels (IL-6 and TNF-α), were quantified in the pleural exudate. In vitro, the effects of <i>trans</i>-cinnamic acid on neutrophil chemotaxis toward CXCL1 were assessed using the Boyden chamber assay. Additionally, human endothelial EA.hy926 cells were stimulated with TNF-α to evaluate neutrophil adhesion and the expression of the adhesion molecule ICAM-1 following <i>trans</i>-cinnamic acid treatment. Pretreatment with <i>trans</i>-cinnamic acid significantly inhibited LPS-induced pleurisy in mice by reducing protein-rich exudate formation, neutrophil infiltration, and local concentrations of TNF-α and IL-6. In vitro, <i>trans</i>-cinnamic acid did not alter CXCL1-induced neutrophil chemotaxis, nor the secretion of CXCL8 produced by TNF-α-stimulated EA.hy926 cells. However, it markedly reduced neutrophil adhesion to TNF-α-activated EA.hy926 cells. This reduction was associated with the downregulation of ICAM-1 expression at both the mRNA and protein levels. Overall, these findings demonstrated that <i>trans</i>-cinnamic acid exerted anti-inflammatory effects by inhibiting vascular permeability and leukocyte recruitment, particularly through the suppression of ICAM-1-mediated neutrophil adhesion to endothelial cells. These results support <i>trans</i>-cinnamic acid as a promising candidate for the development of new therapeutic agents targeting inflammatory diseases.</p> Graphical abstract <p></p>

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Anti-inflammatory effects of trans-cinnamic acid through modulation of endothelial ICAM-1 expression and neutrophil recruitment

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年2月7日

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  • Mark de Sousa Pinheiro Fidelix,
  • Samário Lino Santos,
  • Jordana Rodrigues Santana,
  • Alef Batista Bezerra Barros,
  • Erick Gabriel Alves Ferreira,
  • Graziele Regina Souza Silva,
  • Jamylle Nunes de Souza Ferro,
  • Juliane Pereira Silva,
  • Vincent Lagente,
  • Emiliano Barreto

摘要

Natural phenolic acid compounds have been extensively studied for their anti-inflammatory properties, particularly in the context of inflammation-associated diseases. In this study, we investigated the anti-inflammatory effects of trans-cinnamic acid on neutrophil accumulation during inflammatory processes using both in vivo and in vitro approaches. For the in vivo experiments, LPS-induced pleurisy was used in mice pretreated with trans-cinnamic acid. Inflammatory parameters, including plasma leakage, leukocyte infiltration, and proinflammatory cytokine levels (IL-6 and TNF-α), were quantified in the pleural exudate. In vitro, the effects of trans-cinnamic acid on neutrophil chemotaxis toward CXCL1 were assessed using the Boyden chamber assay. Additionally, human endothelial EA.hy926 cells were stimulated with TNF-α to evaluate neutrophil adhesion and the expression of the adhesion molecule ICAM-1 following trans-cinnamic acid treatment. Pretreatment with trans-cinnamic acid significantly inhibited LPS-induced pleurisy in mice by reducing protein-rich exudate formation, neutrophil infiltration, and local concentrations of TNF-α and IL-6. In vitro, trans-cinnamic acid did not alter CXCL1-induced neutrophil chemotaxis, nor the secretion of CXCL8 produced by TNF-α-stimulated EA.hy926 cells. However, it markedly reduced neutrophil adhesion to TNF-α-activated EA.hy926 cells. This reduction was associated with the downregulation of ICAM-1 expression at both the mRNA and protein levels. Overall, these findings demonstrated that trans-cinnamic acid exerted anti-inflammatory effects by inhibiting vascular permeability and leukocyte recruitment, particularly through the suppression of ICAM-1-mediated neutrophil adhesion to endothelial cells. These results support trans-cinnamic acid as a promising candidate for the development of new therapeutic agents targeting inflammatory diseases.

Graphical abstract