Silymarin component 2,3-dehydrosilybin attenuates cardiomyocyte damage following hypoxia/reoxygenation by limiting oxidative stress
Language English Country Czech Republic Media print-electronic
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
25194130
DOI
10.33549/physiolres.932703
PII: 932703
Knihovny.cz E-resources
- MeSH
- Antioxidants pharmacology MeSH
- Cytoprotection MeSH
- Phosphorylation MeSH
- Ischemic Preconditioning, Myocardial MeSH
- Protein Carbonylation drug effects MeSH
- Myocytes, Cardiac drug effects metabolism pathology MeSH
- Cells, Cultured MeSH
- L-Lactate Dehydrogenase metabolism MeSH
- Animals, Newborn MeSH
- Oxidative Stress drug effects MeSH
- Hydrogen Peroxide metabolism MeSH
- Rats, Wistar MeSH
- Protein Kinase C-epsilon metabolism MeSH
- Myocardial Reperfusion Injury metabolism pathology prevention & control MeSH
- Signal Transduction drug effects MeSH
- Silybin MeSH
- Silymarin pharmacology MeSH
- Cell Survival drug effects MeSH
- Animals MeSH
- Check Tag
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Antioxidants MeSH
- L-Lactate Dehydrogenase MeSH
- Hydrogen Peroxide MeSH
- Prkce protein, rat MeSH Browser
- Protein Kinase C-epsilon MeSH
- Silybin MeSH
- Silymarin MeSH
Ischemic postconditioning and remote conditioning are potentially useful tools for protecting ischemic myocardium. This study tested the hypothesis that 2,3-dehydrosilybin (DHS), a flavonolignan component of Silybum marianum, could attenuate cardiomyocyte damage following hypoxia/reoxygenation by decreasing the generation of reactive oxygen species (ROS). After 5-6 days of cell culture in normoxic conditions the rat neonatal cardiomyocytes were divided into four groups. Control group (9 h at normoxic conditions), hypoxia/reoxygenation group (3 h at 1 % O₂, 94 % N₂and 5 % CO₂followed by 10 min of 10 micromol·l⁻¹DHS and 6 h of reoxygenation in normoxia) and postconditioning group (3 h of hypoxia, three cycles of 5 min reoxygenation and 5 min hypoxia followed by 6 h of normoxia). Cell viability assessed by propidium iodide staining was decreased after DHS treatment consistent with increased levels of lactatedehydrogenase (LDH) after reoxygenation. LDH leakage was significantly reduced when cardiomyocytes in the H/Re group were exposed to DHS. DHS treatment reduced H₂O₂production and also decreased the generation of ROS in the H/Re group as evidenced by a fluorescence indicator. DHS treatment reduces reoxygenation-induced injury in cardiomyocytes by attenuation of ROS generation, H₂O₂and protein carbonyls levels. In addition, we found that both the postconditioning protocol and the DHS treatment are associated with restored ratio of phosphorylated/total protein kinase C epsilon, relative to the H/Re group. In conclusion, our data support the protective role of DHS in hypoxia/reperfusion injury and indicate that DHS may act as a postconditioning mimic.
References provided by Crossref.org
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