ArticlePhotochemistry and photobiology
Silibinin is a potent sensitizer of UVA radiation-induced oxidative stress and apoptosis in human keratinocyte HaCaT cells.
Article in Photochemistry and photobiology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 45 citations in OpenAlex.
- Dysregulation of autophagy during photoaging reduce oxidative stress and inflammatory damage caused by UV.Frontiers in pharmacology · 2025Review
- Silibinin-Loaded Liposomes: The Influence of Modifications on Physicochemical Characteristics, Stability, and Bioactivity Associated with Dermal Application.Pharmaceutics · 2024Article
- IRE1α regulates ROS and immune responses after UVB irradiation.Redox experimental medicine · 2024Article
- Mechanistic Insights into the Pharmacological Significance of Silymarin.Molecules (Basel, Switzerland) · 2022Review
- Glycofullerenes Inhibit Particulate Matter Induced Inflammation and Loss of Barrier Proteins in HaCaT Human Keratinocytes.Biomolecules · 2020Article
- Water-Soluble Fullerenol CInternational journal of molecular sciences · 2019Article
- Silymarin: Friend or Foe of UV Exposed Keratinocytes?Molecules (Basel, Switzerland) · 2019Article
- Keratinocyte Motility Is Affected by UVA Radiation-A Comparison between Normal and Dysplastic Cells.International journal of molecular sciences · 2018Article
- Phytochemicals for the Prevention of Photocarcinogenesis.Photochemistry and photobiology · 2017Review
- Efficacy of Pre- and Post-Treatment by Topical Formulations Containing Dissolved and Suspended Silybum marianum against UVB-Induced Oxidative Stress in Guinea Pig and on HaCaT Keratinocytes.Molecules (Basel, Switzerland) · 2016Article
- Prevention of Photocarcinogenesis by Agonists of 5-HT1A and Antagonists of 5-HT2A Receptors.Molecular neurobiology · 2016Review
- Pro-Oxidant Role of Silibinin in DMBA/TPA Induced Skin Cancer: 1H NMR Metabolomic and Biochemical Study.PloS one · 2016Article
- Saussurea tridactyla Sch. Bip.-derived polysaccharides and flavones reduce oxidative damage in ultraviolet B-irradiated HaCaT cells via a p38MAPK-independent mechanism.Drug design, development and therapy · 2016Article
- An Overview of Ultraviolet B Radiation-Induced Skin Cancer Chemoprevention by Silibinin.Current pharmacology reports · 2015Article
- Purinergic signaling mediates oxidative stress in UVA-exposed THP-1 cells.Toxicology reports · 2015Article
- New Enlightenment of Skin Cancer Chemoprevention through Phytochemicals: In Vitro and In Vivo Studies and the Underlying Mechanisms.BioMed research international · 2014Review
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
UVA radiation (315-400 nm), which constitutes ca 95% of the UV irradiation in natural sunlight reaching earth surface, is a major environmental risk factor associated with human skin cancer pathogenesis. UVA is an oxidizing agent that causes significant damage to cellular components through the release of reactive oxygen species (ROS) and leads to photoaging and photocarcinogenesis. Here we investigate the effect of silibinin, the flavonolignan from Silybum marianum, on UVA-induced ROS and cell death in human keratinocyte cell line HaCaT. In addition, the effect of silibinin on UVA-induced intracellular ROS-mediated endoplasmic reticulum (ER) stress was also analyzed. UVA irradiation resulted in ROS production and apoptosis in HaCaT cells in a dose-dependent manner, and the ROS levels and apoptotic index were found to be elevated significantly when the cells were treated with 75 μmsilibinin for 2 h before UVA exposure. When the cells were pretreated with 10 mmN-acetyl cysteine, the enhancement of UVA-induced apoptosis by silibinin was compromised. Furthermore, we found that silibinin enhances ER stress-mediated apoptosis in HaCaT cells by increasing the expression of CHOP protein. These results suggest that silibinin may be beneficial in the removal of UVA-damaged cells and the prevention of skin cancer.
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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 OpenQuestion graph.