ArticleJournal of natural medicines2026
Anti-inflammatory effects of trans-cinnamic acid through modulation of endothelial ICAM-1 expression and neutrophil recruitment.
Article in Journal of natural medicines, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.