ArticlePloS one2012
Silibinin attenuates sulfur mustard analog-induced skin injury by targeting multiple pathways connecting oxidative stress and inflammation.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 67 citations in OpenAlex.
- Advances in research on the mechanisms of anti-inflammation of silybin: a review.Frontiers in immunology · 2026Review
- Mesna Improves Outcomes of Sulfur Mustard Inhalation Toxicity in an Acute Rat Model.The Journal of pharmacology and experimental therapeutics · 2024Article
- Silymarin and Inflammation: Food for Thoughts.Antioxidants (Basel, Switzerland) · 2024Review
- Article
- Cellular and molecular mechanisms of sulfur mustard toxicity on spermatozoa and male fertility.Toxicology research · 2018Review
- TRPA1 and CGRP antagonists counteract vesicant-induced skin injury and inflammation.Toxicology letters · 2018Article
- Article
- Enhanced migration of murine fibroblast-like 3T3-L1 preadipocytes on type I collagen-coated dish is reversed by silibinin treatment.Molecular and cellular biochemistry · 2018Article
- Silibinin alleviates inflammation and induces apoptosis in human rheumatoid arthritis fibroblast-like synoviocytes and has a therapeutic effect on arthritis in rats.Scientific reports · 2018Article
- Silibinin protects against osteoarthritis through inhibiting the inflammatory response and cartilage matrix degradationOncotarget · 2017Article
- Sulfur mustard inhalation: mechanisms of injury, alteration of coagulation, and fibrinolytic therapy.Annals of the New York Academy of Sciences · 2016Review
- Mustard vesicating agent-induced toxicity in the skin tissue and silibinin as a potential countermeasure.Annals of the New York Academy of Sciences · 2016Review
- Corneal toxicity induced by vesicating agents and effective treatment options.Annals of the New York Academy of Sciences · 2016Review
- Antioxidants as potential medical countermeasures for chemical warfare agents and toxic industrial chemicals.Biochemical pharmacology · 2016Review
- Chemically synthesized CdSe quantum dots inhibit growth of human lung carcinoma cells via ROS generation.EXCLI journal · 2016Article
- Silibinin and its 2,3-dehydro-derivative inhibit basal cell carcinoma growth via suppression of mitogenic signaling and transcription factors activation.Molecular carcinogenesis · 2016Article
- Pro-Oxidant Role of Silibinin in DMBA/TPA Induced Skin Cancer: 1H NMR Metabolomic and Biochemical Study.PloS one · 2016Article
- The Mixture of Salvianolic Acids from Salvia miltiorrhiza and Total Flavonoids from Anemarrhena asphodeloides Attenuate Sulfur Mustard-Induced Injury.International journal of molecular sciences · 2015Article
- Silibinin attenuates methotrexate-induced pulmonary injury by targeting oxidative stress.Experimental and therapeutic medicine · 2015Article
- Cissus quadrangularis Linn exerts dose-dependent biphasic effects: osteogenic and anti-proliferative, through modulating ROS, cell cycle and Runx2 gene expression in primary rat osteoblasts.Cell proliferation · 2015Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Chemical warfare agent sulfur mustard (HD) inflicts delayed blistering and incapacitating skin injuries. To identify effective countermeasures against HD-induced skin injuries, efficacy studies were carried out employing HD analog 2-chloroethyl ethyl sulfide (CEES)-induced injury biomarkers in skin cells and SKH-1 hairless mouse skin. The data demonstrate strong therapeutic efficacy of silibinin, a natural flavanone, in attenuating CEES-induced skin injury and oxidative stress. In skin cells, silibinin (10 µM) treatment 30 min after 0.35/0.5 mM CEES exposure caused a significant (p<0.05) reversal in CEES-induced decrease in cell viability, apoptotic and necrotic cell death, DNA damage, and an increase in oxidative stress. Silibinin (1 mg) applied topically to mouse skin 30 min post-CEES exposure (2 mg), was effective in reversing CEES-induced increases in skin bi-fold (62%) and epidermal thickness (85%), apoptotic cell death (70%), myeloperoxidase activity (complete reversal), induction of iNOS, COX-2, and MMP-9 protein levels (>90%), and activation of transcription factors NF-κB and AP-1 (complete reversal). Similarly, silibinin treatment was also effective in attenuating CEES-induced oxidative stress measured by 4-hydroxynonenal and 5,5-dimethyl-2-(8-octanoic acid)-1-pyrolline N-oxide protein adduct formation, and 8-oxo-2-deoxyguanosine levels. Since our previous studies implicated oxidative stress, in part, in CEES-induced toxic responses, the reversal of CEES-induced oxidative stress and other toxic effects by silibinin in this study indicate its pleiotropic therapeutic efficacy. Together, these findings support further optimization of silibinin in HD skin toxicity model to develop a novel effective therapy for skin injuries by vesicants.
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