Antioxidative Effects of Cherry Leaves Extract on tert-Butyl Hydroperoxide-Mediated Cytotoxicity Through Regulation of Thioredoxin-2 Protein Expression Levels
| Autor: | Yuji Goto, Noriyuki Uemura, Masanao Niwa, Kazuhiro Hara, Daisuke Watanabe, Takeshi Yanagishita, Nobuhiko Taguchi, Masaaki Sakura, Masashi Kato, Machiko Iida |
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| Rok vydání: | 2011 |
| Předmět: |
Programmed cell death
Cell Survival DNA damage Health Toxicology and Mutagenesis p38 mitogen-activated protein kinases Biology Toxicology p38 Mitogen-Activated Protein Kinases Antioxidants Cell Line Mitochondrial Proteins chemistry.chemical_compound Thioredoxins tert-Butylhydroperoxide Humans chemistry.chemical_classification Reactive oxygen species Plant Extracts fungi Glutathione Oxidants metropolitan_transit.transit_stop Up-Regulation Enzyme Activation Plant Leaves Oxidative Stress chemistry Biochemistry tert-Butyl hydroperoxide Melanocytes Prunus metropolitan_transit Thioredoxin Reactive Oxygen Species Cherry tree DNA Damage Phytotherapy Signal Transduction |
| Zdroj: | Journal of Toxicology and Environmental Health, Part A. 74:1240-1247 |
| ISSN: | 1087-2620 1528-7394 |
| DOI: | 10.1080/15287394.2011.570229 |
| Popis: | Components of cherry trees have been used as traditional herbal remedies for various diseases. These components are known to possess antioxidative effects. However, the mechanisms underlying cherry tree component-mediated antioxidative effects remain largely unknown. This study focused on cherry leaves extract (CLE) and examined the mechanism underlying the effect of CLE on tert-butyl hydroperoxide (t-BOOH)-induced melanocytic cell death with DNA damage. Interestingly, CLE prevented t-BOOH-induced cell death with reduction in DNA damage, p38 kinase activation, and reactive oxygen species (ROS) production. CLE-mediated suppression of cell death with reduction of DNA damage, p38 kinase activity and ROS production was prevented by a thioredoxin (Trx) system inhibitor but not by a glutathione (GSH) system inhibitor. Finally, data showed that CLE prevented t-BOOH-induced reduction of Trx2 but not Trx1 and Trx reductases (TrxR1 and TrxR2) protein expression. Thus, our results suggest that CLE prevents t-BOOH-induced reduction in Trx2 expression, promotion of ROS production, activation of p38 kinase, and increase in DNA damage and that it protects against cell death. |
| Databáze: | OpenAIRE |
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