ArticleInflammopharmacology2025
Fenchone attenuates CD68-dependent 7-ketocholesterol accumulation, cholesterol dyshomeostasis and inflammatory responses via modulation of macrophage polarization.
Article in Inflammopharmacology, 2025. 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
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundFoam cell formation, driven by oxidized low-density lipoprotein (Ox-LDL) uptake, particularly 7-ketocholesterol (7KCh), is a pivotal event in lipid-associated inflammatory diseases such as atherosclerosis. Conventional therapies often yield side effects, prompting interest in plant-derived biomolecules. Fenchone, a monoterpene from Foeniculum vulgare, has recently garnered attention for its anti-inflammatory and anti-lipidemic potential. PURPOSE: This study elucidates the pharmacologic efficacy of fenchone in mitigating foam cell formation by modulating cholesterol homeostasis, inflammatory signaling and polarization in macrophages.
methodsMurine IC-21 macrophages were induced with 7KCh and co-treated with fenchone. Cell viability was assessed using alamar blue assay, while lipid and calcium accumulation were analyzed with oil red O and alizarin red S staining. Pinocytosis, phagocytosis and actin cytoskeleton were evaluated with neutral red, goat RBCs uptake and phalloidin, respectively. Molecular changes were determined using ELISA, flow cytometry, PCR, western blot and in silico docking.
resultsFenchone significantly inhibited lipid and calcium accumulation, reduced lipid peroxidation and restored homeostatic endocytosis with anti-inflammatory cytoskeleton. It enhanced anti-inflammatory TGFβ1 and Smad2/3 while suppressing pro-inflammatory NF-κB, IL-1β, IL-6 and TNF-α. In addition, fenchone regulated cholesterol homeostasis via ABCA1, ApoE, LXR, CD36 and promoted M2 polarization by increasing CD163 and CD206 markers, downregulating M1 markers (CD38, CD68 and CD86). Computational analysis indicated the interactive affinity of 7KCh toward the CD68 scavenger receptor, which was prevented by fenchone.
conclusionThese findings highlight the therapeutic potential of fenchone in managing atherosclerosis by targeting CD68-mediated 7KCh uptake and inflammatory cascade, thereby emerging as a potential pharmacotherapeutic agent in inflammatory diseases.
Indexed as
Identifiers
40591211What Socratic 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 Socratic graph.