Artemisinin attenuates doxorubicin induced cardiotoxicity and hepatotoxicity in rats
| Autor: | Hidayet Tutun, Alper Yalcin, Ibrahim Aktas, Ozlem Ozmen, Ahmet Türk |
|---|---|
| Rok vydání: | 2019 |
| Předmět: |
Male
0301 basic medicine Histology Apoptosis Caspase 3 macromolecular substances Pharmacology Antioxidants Rats Sprague-Dawley 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Untreated control Male rats polycyclic compounds Animals Medicine Doxorubicin Artemisinin Inflammation Cardiotoxicity Antibiotics Antineoplastic 030102 biochemistry & molecular biology business.industry Myocardium organic chemicals technology industry and agriculture NF-κB General Medicine Artemisinins carbohydrates (lipids) Oxidative Stress Medical Laboratory Technology chemistry 030220 oncology & carcinogenesis business Liver pathology medicine.drug |
| Zdroj: | Biotechnic & Histochemistry. 95:121-128 |
| ISSN: | 1473-7760 1052-0295 |
| Popis: | We investigated the effects of artemisinin on doxorubicin (Dox) induced heart and liver pathology in rats. We divided 49 male rats into seven groups: group 1 was the untreated control. Dox was administered intraperitoneally to groups 2, 3 and 4 on day 1. Artemisinin was administered by gavage to groups 3 and 6 at a dose of 7 mg/kg, and to groups 4 and 7 at a dose of 35 mg/kg for 14 days. Group 5 was given only 0.9% NaCl orally for 14 days. At the end of the study, heart and liver samples were collected for histopathology and immunohistochemistry. Hyperemia and slight hemorrhages were observed in both livers and hearts of rats treated with Dox only. Significant increases in caspase-3, TNF-α, iNOS and NF-κB expression were observed in the myocardial cells and hepatocytes of group 2. Significant reductions in caspase-3, TNF-α, iNOS and NF-κB expression were observed in groups 3 and 4 following artemisinin treatment compared to group 2. Artemisinin may exert protective effects against Dox induced cardiotoxicity and hepatotoxicity in rats. |
| Databáze: | OpenAIRE |
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