Mesenchymal stem cells pretreated with platelet-rich plasma modulate doxorubicin-induced cardiotoxicity
| العنوان: | Mesenchymal stem cells pretreated with platelet-rich plasma modulate doxorubicin-induced cardiotoxicity |
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| المؤلفون: | Sherif Mohamed Zaki, M M Abdelmoaty, Wa Abd Algaleel, R A Imam |
| المصدر: | Human & Experimental Toxicology. 38:857-874 |
| بيانات النشر: | SAGE Publications, 2019. |
| سنة النشر: | 2019 |
| مصطلحات موضوعية: | Male, 0301 basic medicine, Health, Toxicology and Mutagenesis, Apoptosis, Inflammation, Pharmacology, Toxicology, medicine.disease_cause, 03 medical and health sciences, chemistry.chemical_compound, 0302 clinical medicine, Malondialdehyde, medicine, Animals, Creatine Kinase, MB Form, Rats, Wistar, Cardiotoxicity, Antibiotics, Antineoplastic, Platelet-Rich Plasma, Superoxide Dismutase, Tumor Necrosis Factor-alpha, Myocardium, Mesenchymal stem cell, Mesenchymal Stem Cells, General Medicine, Interleukin-10, Vascular endothelial growth factor, Oxidative Stress, 030104 developmental biology, chemistry, Doxorubicin, 030220 oncology & carcinogenesis, Platelet-rich plasma, Tumor necrosis factor alpha, medicine.symptom, Oxidative stress |
| الوصف: | The cardiotoxic adverse effect of doxorubicin (DOX) is the major factor limiting its use. Recently, mesenchymal stem cells (MSCs) have been implicated in the preclinical studies of treatment of DOX-induced cardiotoxicity. The question is MSCs pretreated with platelet-rich plasma (PRP) have a better influence on DOX-induced cardiotoxicity compared to the influence of MSCs alone. Twenty-four Wistar rats were categorized into control, DOX-treated, MSC-treated, and PRP/MSC-treated groups. DOX was injected for two consecutive weeks. Light microscopic, biochemical markers (interleukin 10 (IL-10), tumor necrosis factor alpha (TNF-α), and creatine kinase-MB (CK-MB)), immunohistochemical (Bax, Bcl2, vascular endothelial growth factor (VEGF), and cardiac troponin-I (CT-I)), and oxidative/antioxidative markers (malondialdehyde (MDA)/superoxide dismutase (SOD)) were measured. Degenerative cardiac changes were detected in the DOX-treated group with complete loss of the architecture and coagulative necrosis. These changes were accompanied with the elevation of the serum level of CK-MB and loss of CT-I immunoreactivity. The major factors in the DOX-induced cardiotoxicity were the oxidative stress (elevated MDA/decreased SOD), inflammation (elevated TNF-α/decreased IL-10), and cardiac apoptosis (lower Bcl2, higher Bax, and lower Bcl2/Bax ratio). MSCs and PRP/MSCs attenuate DOX-induced cardiotoxicity. Better attenuation was observed in the PRP/MSC-treated group. PRP/MSC combination reduced greatly the MDA and TNF-α and increased IL-10, Bcl2/Bax ratio, and VEGF. PRP had no significant influence over the Bcl2, Bax, and SOD. In conclusion, DOX in its toxic dose induced myocardial injury. This destructive effect is related to oxidative stress, inflammation, and cardiac apoptosis. PRP/MSC possesses a better attenuation over the DOX-induced toxicity compared to MSC alone. |
| تدمد: | 1477-0903 0960-3271 |
| URL الوصول: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::314cd1ac32433a28167bdf706200bd5c https://doi.org/10.1177/0960327119842613 |
| حقوق: | CLOSED |
| رقم الأكسشن: | edsair.doi.dedup.....314cd1ac32433a28167bdf706200bd5c |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 14770903 09603271 |
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