ArticleToxicology and applied pharmacology2012
Silibinin, dexamethasone, and doxycycline as potential therapeutic agents for treating vesicant-inflicted ocular injuries.
Article in Toxicology and applied pharmacology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 52 citations in OpenAlex.
- BRD4 inhibition mitigates acute and chronic corneal injury following topical nitrogen mustard exposure.Molecular therapy : the journal of the American Society of Gene Therapy · 2026Article
- Current progress in research on ocular injury caused by exposure to vesicants.Progress in retinal and eye research · 2025Review
- Article
- Dexamethasone sodium phosphate loaded nanoparticles for prevention of nitrogen mustard induced corneal injury.Experimental eye research · 2024Article
- Chloropicrin induced ocular injury: Biomarkers, potential mechanisms, and treatments.Toxicology letters · 2024Review
- Nitrogen Mustard-Induced Ex Vivo Human Cornea Injury Model and Therapeutic Intervention by Dexamethasone.The Journal of pharmacology and experimental therapeutics · 2024Article
- Establishing a Dexamethasone Treatment Regimen To Alleviate Sulfur Mustard-Induced Corneal Injuries in a Rabbit Model.The Journal of pharmacology and experimental therapeutics · 2024Article
- Article
- Phenylarsine oxide induced corneal injury involves oxidative stress mediated unfolded protein response and ferroptotic cell death: Amelioration by NAC.Free radical biology & medicine · 2023Article
- Ocular injury progression and cornea histopathology from chloropicrin vapor exposure: Relevant clinical biomarkers in mice.Experimental eye research · 2023Article
- Progress towards a standardized model of ocular sulfur mustard injury for therapeutic testing.Experimental eye research · 2023Article
- Sulfur mustard corneal injury is associated with alterations in the epithelial basement membrane and stromal extracellular matrix.Experimental and molecular pathology · 2022Article
- Therapeutic Potential of Mesenchymal Stem Cell-Secreted Factors on Delay in Corneal Wound Healing by Nitrogen Mustard.International journal of molecular sciences · 2022Article
- Effect of dexamethasone treatment at variable therapeutic windows in reversing nitrogen mustard-induced corneal injuries in rabbit ocular in vivo model.Toxicology and applied pharmacology · 2022Article
- Possible treatment with medicinal herbs and their ingredients of lung disorders induced by sulfur mustard exposures: a review.Environmental science and pollution research international · 2021Review
- Ocular toxicity of mustard gas: A concise review.Toxicology letters · 2021Review
- Pathophysiology and inflammatory biomarkers of sulfur mustard-induced corneal injury in rabbits.PloS one · 2021Article
- Considerations in developing medical countermeasures against chemical ocular toxicity.Toxicology letters · 2020Article
- A Novel Topical Ophthalmic Formulation to Mitigate Acute Mustard Gas Keratopathy In Vivo: A Pilot Study.Translational vision science & technology · 2020Article
- Acute corneal injury in rabbits following nitrogen mustard ocular exposure.Experimental and molecular pathology · 2019Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
There are no effective and approved therapies against devastating ocular injuries caused by vesicating chemical agents sulfur mustard (SM) and nitrogen mustard (NM). Herein, studies were carried out in rabbit corneal cultures to establish relevant ocular injury biomarkers with NM for screening potential efficacious agents in laboratory settings. NM (100nmol) exposure of the corneas for 2h (cultured for 24h), showed increases in epithelial thickness, ulceration, apoptotic cell death, epithelial detachment microbullae formation, and the levels of VEGF, cyclooxygenase-2 (COX-2) and matrix metalloproteinase-9 (MMP-9). Employing these biomarkers, efficacy studies were performed with agent treatments 2h and every 4h thereafter, for 24h following NM exposure. Three agents were evaluated, including prescription drugs dexamethasone (0.1%; anti-inflammatory steroid) and doxycycline (100nmol; antibiotic and MMP inhibitor) that have been studied earlier for treating vesicant-induced eye injuries. We also examined silibinin (100μg), a non-toxic natural flavanone found to be effective in treating SM analog-induced skin injuries in our earlier studies. Treatments of doxycycline+dexamethasone, and silibinin were more effective than doxycycline or dexamethasone alone in reversing NM-induced epithelial thickening, microbullae formation, apoptotic cell death, and MMP-9 elevation. However, dexamethasone and silibinin alone were more effective in reversing NM-induced VEGF levels. Doxycycline, dexamethasone and silibinin were all effective in reversing NM-induced COX-2 levels. Apart from therapeutic efficacy of doxycycline and dexamethasone, these results show strong multifunctional efficacy of silibinin in reversing NM-induced ocular injuries, which could help develop effective and safe therapeutics against ocular injuries by vesicants.
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