ArticleMolecular biology reports2026
Xanthium strumarium L. extract attenuates TNF-α/IFN-γ- stimulated inflammation and promotes hyaluronan production on HaCaT keratinocytes.
Article in Molecular biology reports, 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
8 authors.
Funding
Abstract
backgroundXanthium strumarium L. has traditionally been used for inflammatory disorders; however, its molecular effects on keratinocyte inflammation and hyaluronan metabolism remain poorly understood. This study evaluated the modulatory trends of X.strumarium L. extract (XsE) on TNF-α/IFN-γ-stimulated inflammatory signaling pathway and hyaluronan regulation on HaCaT keratinocytes. METHODS AND
resultsThe antioxidative stress of XsE was evaluated by free radical scavenging assays and dichlorofluorescein fluorescence staining. XsE exhibited significant antioxidant activity without inducing cytotoxicity in HaCaT cells and markedly attenuated TNF-α/IFN-γ-induced ROS accumulation. The gene expression and ELISA assays revealed that XsE suppressed pro-inflammatory cytokines and chemokines, including IL-6, IL-8, TARC, RANTES, and CTACK, at both transcriptional and protein levels. Mechanistically, Western blot analysis demonstrated that XsE treatment was strongly associated with the suppression of p38, IκBα, and p65 phosphorylation within the canonical NF-κB and specific p38 MAPK signaling cascades. In addition, XsE enhanced hyaluronan accumulation by upregulating hyaluronan synthase gene transcription, resulting in verified downstream macromolecule secretion. UPLC-MS analysis identified chlorogenic acid, miquelianin, hyperoside, cynarine, and syringetin as major phytochemical constituents in XsE. Molecular docking analysis further supported the predicted interactions of these compounds with inflammation- and hyaluronan-related targets.
conclusionsThese findings demonstrate that the anti-inflammatory and hyaluronan-producing properties of XsE may contribute to the regulation of epidermal inflammatory responses and skin barrier-associated functions.
Indexed as
Identifiers
42663725What 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.