ArticleToxicology and applied pharmacology2014
Therapeutic potential of a non-steroidal bifunctional anti-inflammatory and anti-cholinergic agent against skin injury induced by sulfur mustard.
Article in Toxicology and applied pharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 24 citations in OpenAlex.
- A standardized in vitro bioengineered skin for penetrating wound modeling.In vitro models · 2025Article
- Optimizing Nanosuspension Drug Release and Wound Healing Using a Design of Experiments Approach: Improving the Drug Delivery Potential of NDH-4338 for Treating Chemical Burns.Pharmaceutics · 2024Article
- Expression of Laminin γ2 Proteolytic Fragments in Murine Skin Following Exposure to Sulfur Mustard.Anatomical record (Hoboken, N.J. : 2007) · 2020Article
- Expression of cytokines and chemokines in mouse skin treated with sulfur mustard.Toxicology and applied pharmacology · 2018Article
- Sulfur mustard induced mast cell degranulation in mouse skin is inhibited by a novel anti-inflammatory and anticholinergic bifunctional prodrug.Toxicology letters · 2018Article
- Defining the timing of 25(OH)D rescue following nitrogen mustard exposure.Cutaneous and ocular toxicology · 2018Article
- Scar management in burn injuries using drug delivery and molecular signaling: Current treatments and future directions.Advanced drug delivery reviews · 2018Review
- Expression of Laminin 332 in Vesicant Skin Injury and Wound Repair.Clinical dermatology (Wilmington, Del.) · 2018Article
- Development, Optimization and In Vitro/In Vivo Characterization of Collagen-Dextran Spongious Wound Dressings Loaded with Flufenamic Acid.Molecules (Basel, Switzerland) · 2017Article
- Multi-inhibitor prodrug constructs for simultaneous delivery of anti-inflammatory agents to mustard-induced skin injury.Annals of the New York Academy of Sciences · 2016Review
- Tissue injury and repair following cutaneous exposure of mice to sulfur mustard.Annals of the New York Academy of Sciences · 2016Review
- Mustard vesicants alter expression of the endocannabinoid system in mouse skin.Toxicology and applied pharmacology · 2016Article
- Emerging targets for treating sulfur mustard-induced injuries.Annals of the New York Academy of Sciences · 2016Review
- Mitigation of nitrogen mustard mediated skin injury by a novel indomethacin bifunctional prodrug.Experimental and molecular pathology · 2016Article
- Flavanone silibinin treatment attenuates nitrogen mustard-induced toxic effects in mouse skin.Toxicology and applied pharmacology · 2015Article
Corrections and comments
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Authors and funding
13 authors at 5 institutions in 1 country.
Funding
Abstract
Sulfur mustard (bis(2-chloroethyl) sulfide, SM) is a highly reactive bifunctional alkylating agent inducing edema, inflammation, and the formation of fluid-filled blisters in the skin. Medical countermeasures against SM-induced cutaneous injury have yet to be established. In the present studies, we tested a novel, bifunctional anti-inflammatory prodrug (NDH 4338) designed to target cyclooxygenase 2 (COX2), an enzyme that generates inflammatory eicosanoids, and acetylcholinesterase, an enzyme mediating activation of cholinergic inflammatory pathways in a model of SM-induced skin injury. Adult SKH-1 hairless male mice were exposed to SM using a dorsal skin vapor cup model. NDH 4338 was applied topically to the skin 24, 48, and 72 h post-SM exposure. After 96 h, SM was found to induce skin injury characterized by edema, epidermal hyperplasia, loss of the differentiation marker, keratin 10 (K10), upregulation of the skin wound marker keratin 6 (K6), disruption of the basement membrane anchoring protein laminin 322, and increased expression of epidermal COX2. NDH 4338 post-treatment reduced SM-induced dermal edema and enhanced skin re-epithelialization. This was associated with a reduction in COX2 expression, increased K10 expression in the suprabasal epidermis, and reduced expression of K6. NDH 4338 also restored basement membrane integrity, as evidenced by continuous expression of laminin 332 at the dermal-epidermal junction. Taken together, these data indicate that a bifunctional anti-inflammatory prodrug stimulates repair of SM induced skin injury and may be useful as a medical countermeasure.
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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.