ArticleGenes & genomics2021
Glabridin attenuates atopic dermatitis progression through downregulating the TLR4/MyD88/NF-κB signaling pathway.
Article in Genes & genomics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.
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
12 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.
- Glutamine Peptides: Preparation, Analysis, Applications, and Their Role in Intestinal Barrier Protection.Nutrients · 2025Pooled it
- A Narrative Review of the Multi-Target Mechanisms of Glabridin in Skin Lightening.Clinical, cosmetic and investigational dermatology · 2026Review
- Anti-Inflammatory Activity of Compounds Isolated fromInternational journal of molecular sciences · 2025Article
- Optimization ultrasonic-assisted aqueous two-phase extraction of glabridin from licorice root and its activity against the foodborne pathogen MRSA.Food chemistry: X · 2025Article
- Glabridin Suppresses Macrophage Activation by Lipoteichoic Acid In Vitro: The Crucial Role of MAPKs-IL-1β-iNOS Axis Signals in Peritoneal and Alveolar Macrophages.Biomolecules · 2025Article
- Skin Microbiome in Health and Disease: Mechanisms and Emerging Therapeutic Strategies.Clinical, cosmetic and investigational dermatology · 2025Review
- Metabolomics analyses reveal the crucial role of ERK in regulating metabolic pathways associated with the proliferation of human cutaneous T-cell lymphoma cells treated with Glabridin.Cell proliferation · 2024Article
- Jianpi Yangxue Qufeng compound alleviates atopic dermatitis via TLR4/MyD88/NF-κB signaling pathway.Heliyon · 2024Article
- The anti-inflammatory activity of GABA-enrichedFrontiers in nutrition · 2023Article
- Review on the Diverse Biological Effects of Glabridin.Drug design, development and therapy · 2023Review
- Article
- Osthole Regulates Secretion of Pro-Inflammatory Cytokines and Expression ofJournal of inflammation research · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundGlabridin (GB), a bio-available phytoestrogen, displays various biological properties such as anti-inflammatory, antibacterial, and antiviral.
objectiveTo explore the role of GB in the process of atopic dermatitis (AD).
methodsCCK8 was used to detect the therapeutic effect of Glabridin in HaCat and NHEK cell inflammatory models. And evaluated the effect on cell proliferation and cell viability. The expression of TLR4, MyD88, P65 and P50 in HaCat and NHEK cell tissues was detected by qRT-PCR and PCR. At the same time, an AD animal model was constructed, and the cell experiment results were verified by hematoxylin-eosin (HE) and Immunohistochemistry staining (IHC).
resultsEnzyme-linked immunosorbent assay (ELISA) demonstrated that IL-1β, IL-6, and TNF-α upregulated by lipopolysaccharide (LPS) was decreased by treatment with GB. AD progression was further confirmed to be regulated by GB by inhibiting the TLR4/MyD88/NF-κB signaling pathway through real-time PCR and Western blot analyses. An AD-like mouse model demonstrated that GB considerably alleviated epidermal injury, relieve edema, and reduced inflammatory cell infiltration by H&E staining. Concurrently, IHC staining exhibited GB to reduce AD progression by impeding TLR4 expression.
conclusionGB was observed to decrease the AD progression by suppressing the TLR4/MyD88/NF-κB signaling pathway, which may likely serve as a novel therapeutic drug for AD management.
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.