In Vivo Protective Effects of Diosgenin against Doxorubicin-Induced Cardiotoxicity
| Autor: | Jing-Hsien Chen, Hui-Hsuan Lin, Chih-Tai Chen, Cheng-Chin Hsu, Zhi-Hong Wang |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2015 |
| Předmět: |
Male
antioxidant lcsh:TX341-641 Apoptosis Blood Pressure Pharmacology Diosgenin medicine.disease_cause doxorubicin Thiobarbituric Acid Reactive Substances Article Antioxidants Superoxide dismutase chemistry.chemical_compound Mice Heart Rate TBARS medicine Animals Creatine Kinase chemistry.chemical_classification Reactive oxygen species Cardiotoxicity Glutathione Peroxidase Mice Inbred BALB C Nutrition and Dietetics biology L-Lactate Dehydrogenase Caspase 3 Dioscorea Plant Extracts Superoxide Dismutase Glutathione peroxidase cadiotoxicity cGMP Oxidative Stress chemistry biology.protein Creatine kinase Cardiomyopathies Reactive Oxygen Species lcsh:Nutrition. Foods and food supply Oxidative stress Biomarkers Food Science |
| Zdroj: | Nutrients Volume 7 Issue 6 Pages 4938-4954 Nutrients, Vol 7, Iss 6, Pp 4938-4954 (2015) |
| ISSN: | 2072-6643 |
| Popis: | Doxorubicin (DOX) induces oxidative stress leading to cardiotoxicity. Diosgenin, a steroidal saponin of Dioscorea opposita, has been reported to have antioxidant activity. Our study was aimed to find out the protective effect of diosgenin against DOX-induced cardiotoxicity in mice. DOX treatment led to a significant decrease in the ratio of heart weight to body weight, and increases in the blood pressure and the serum levels of lactate dehydrogenase (LDH), creatine phosphokinase (CPK) and creatine kinase myocardial bound (CK-MB), markers of cardiotoxicity. In the heart tissue of the DOX-treated mice, DOX reduced activities of antioxidant enzymes, including superoxide dismutase (SOD) and glutathione peroxidase (GPx), were recovered by diosgenin. Diosgenin also decreased the serum levels of cardiotoxicity markers, cardiac levels of thiobarbituric acid relative substances (TBARS) and reactive oxygen species (ROS), caspase-3 activation, and mitochondrial dysfunction, as well as the expression of nuclear factor kappa B (NF-κB), an inflammatory factor. Moreover, diosgenin had the effects of increasing the cardiac levels of cGMP via modulation of phosphodiesterase-5 (PDE5) activity, and in improving myocardial fibrosis in the DOX-treated mice. Molecular data showed that the protective effects of diosgenin might be mediated via regulation of protein kinase A (PKA) and p38. Our data imply that diosgenin possesses antioxidant and anti-apoptotic activities, and cGMP modulation effect, which in turn protect the heart from the DOX-induced cardiotoxicity. |
| Databáze: | OpenAIRE |
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