ArticleMolecular medicine reports2026
Glabridin attenuates LTA‑induced alveolar macrophage migration via activation of the Nrf2/HO‑1 pathway.
Article in Molecular medicine 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
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Oxidative stress and macrophage migration contribute to chronic inflammation and resultant tissue damage. The nuclear factor erythroid 2‑related factor 2 (Nrf2) antioxidant pathway plays a key role in maintaining redox balance and modulating immune cell behavior. Lipoteichoic acid (LTA), a component of Gram‑positive bacterial membranes, activates macrophages and overproduces reactive oxygen species (ROS), causing oxidative stress and aberrant macrophage migration. In the present study, the effects of glabridin (GBD), a flavonoid from licorice with antioxidant potential, on LTA‑mediated oxidative stress and alveolar macrophage migration were investigated. GBD pretreatment reduced intracellular ROS levels, as measured through 2',7'‑dichlorofluorescin diacetate and dihydroethidium staining. Immunofluorescence microscopy revealed increased nuclear translocation of Nrf2 following GBD treatment. Western blotting demonstrated elevated expression of Nrf2 and its downstream target, heme oxygenase‑1 (HO‑1). Cotreatment with the Nrf2 inhibitor ML385 attenuated GBD‑mediated Nrf2 activation and HO‑1 expression, suggesting involvement of the Nrf2/HO‑1 pathway. Functionally, GBD inhibited LTA‑induced macrophage migration, and this effect was attenuated by ML385 cotreatment. These findings demonstrate that GBD suppresses LTA‑induced macrophage migration, at least in part, through the Nrf2/HO‑1 signaling pathway, suggesting potential therapeutic relevance in inflammatory lung diseases.
Indexed as
Identifiers
What 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.