ArticleFrontiers in immunology2019
GSH-C4 Acts as Anti-inflammatory Drug in Different Models of Canonical and Cell Autonomous Inflammation Through NFκB Inhibition.
Article in Frontiers in immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. It is linked to trial NCT07433907 (A Prospective, Randomized, Split-Face Pilot Study Comparing the Efficacy of the Institute of Dermatology's Antioxidant Moisturizing Serum in Mild to Moderate Seborrheic Dermatitis), which is not on this map. Cited by 21 papers.
What it found
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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.
A Prospective, Randomized, Split-Face Pilot Study Comparing the Efficacy of the Institute of Dermatology's Antioxidant Moisturizing Serum in Mild to Moderate Seborrheic Dermatitis
Who cites it
21 citing papers in PubMed, 32 citations in OpenAlex.
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- Glutathione-Mediated Redox Regulation of Immune Dysfunction in COVID-19 and Tuberculosis.Antioxidants (Basel, Switzerland) · 2026Review
- Efficacy of hyaluronic acid and butyroyl glutathione in the management of glaucoma-related ocular surface disease: a prospective, interventional, double-blind, cross-over post market study.Frontiers in pharmacology · 2026Article
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- Glutathione: A Key Regulator of Extracellular Matrix and Cell Death in Intervertebral Disc Degeneration.Mediators of inflammation · 2024Review
- The circadian rhythm gene Bmal1 ameliorates acute deoxynivalenol-induced liver damage.Archives of toxicology · 2023Article
- Oxidative Stress in Traumatic Brain Injury.International journal of molecular sciences · 2022Review
- Gold Nanoclusters Display Low Immunogenic Effect in Microglia Cells.Nanomaterials (Basel, Switzerland) · 2021Article
- Silencing TLR4/MyD88/NF-κB Signaling Pathway Alleviated Inflammation of Corneal Epithelial Cells Infected by ISE.Inflammation · 2021Article
- Intracellular Redox-Modulated Pathways as Targets for Effective Approaches in the Treatment of Viral Infection.International journal of molecular sciences · 2021Review
- Reprograming of Tumor-Associated Macrophages in Breast Tumor-Bearing Mice under Chemotherapy by Targeting Heme Oxygenase-1.Antioxidants (Basel, Switzerland) · 2021Article
- Oleuropein Aglycone Peracetylated (3,4-DHPEA-EA(P)) Attenuates HMolecules (Basel, Switzerland) · 2020Article
- Glutathione Supplementation as an Adjunctive Therapy in COVID-19.Antioxidants (Basel, Switzerland) · 2020Review
- Redox control in the pathophysiology of influenza virus infection.BMC microbiology · 2020Review
- Antioxidant Therapies in Traumatic Brain Injury.Antioxidants (Basel, Switzerland) · 2020Review
- Flavonoid-mediated immunomodulation of human macrophages involves key metabolites and metabolic pathways.Scientific reports · 2019Article
- Glutathione and Nitric Oxide: Key Team Players in Use and Disuse of Skeletal Muscle.Nutrients · 2019Review
Corrections and comments
- Erratum issued
Authors and funding
9 authors at 7 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
An imbalance in GSH/GSSG ratio represents a triggering event in pro-inflammatory cytokine production and inflammatory response. However, the molecular mechanism(s) through which GSH regulates macrophage and cell autonomous inflammation remains not deeply understood. Here, we investigated the effects of a derivative of GSH, the N-butanoyl glutathione (GSH-C4), a cell permeable compound, on lipopolisaccharide (LPS)-stimulated murine RAW 264.7 macrophages, and human macrophages. LPS alone induces a significant production of pro-inflammatory cytokines, such as IL-1β, IL-6, and TNF-α and a significant decrement of GSH content. Such events were significantly abrogated by treatment with GSH-C4. Moreover, GSH-C4 was highly efficient in buffering cell autonomous inflammatory status of aged C2C12 myotubes and 3T3-L1 adipocytes by suppressing the production of pro-inflammatory cytokines. We found that inflammation was paralleled by a strong induction of the phosphorylated form of NFκB, which translocates into the nucleus; a process that was also efficiently inhibited by the treatment with GSH-C4. Overall, the evidence suggests that GSH decrement is required for efficient activation of an inflammatory condition and, at the same time, GSH-C4 can be envisaged as a good candidate to abrogate such process, expanding the anti-inflammatory role of this molecule in chronic inflammatory states.
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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.