Forskolin attenuates doxorubicin-induced accumulation of asymmetric dimethylarginine and s-adenosylhomocysteine via methyltransferase activity in leukemic monocytes
| Autor: | Ganesh Munuswamy-Ramanujan, Kanchana Mala, Vinnie Cheeran, Sandhiya Ramachandran, Swetha Loganathan, Vijay Raj, Mohankumar Ramasamy, Soniya Charles |
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| Rok vydání: | 2018 |
| Předmět: |
0301 basic medicine
Methyltransferase macromolecular substances Pharmacology lcsh:RC254-282 03 medical and health sciences chemistry.chemical_compound polycyclic compounds medicine Cytotoxic T cell Doxorubicin Endothelial dysfunction Cytotoxicity Forskolin business.industry organic chemicals technology industry and agriculture Hematology lcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens medicine.disease Metformin carbohydrates (lipids) 030104 developmental biology Oncology chemistry Asymmetric dimethylarginine business medicine.drug |
| Zdroj: | Leukemia Research Reports, Vol 9, Iss, Pp 28-35 (2018) |
| ISSN: | 2213-0489 |
| Popis: | Doxorubicin (DOX) is an antitumor drug, associated with cardiomyopathy. Strategies to address DOX-cardiomyopathy are scarce. Here, we identify the effect of forskolin (FSK) on DOX-induced-asymmetric-dimethylarginine (ADMA) accumulation in monocytoid cells. DOX-challenge led to i) augmented cytotoxicity, reactive-oxygen-species (ROS) production and methyltransferase-enzyme-activity identified as ADMA and s-adenosylhomocysteine (SAH) accumulation (SAH-A). However, except cytotoxicity, other DOX effects were decreased by metformin and FSK. FSK, did not alter the DOX-induced cytotoxic effect, but, decreased SAH-A by >50% and a combination of three drugs restored physiological methyltransferase-enzyme-activity. Together, protective effect of FSK against DOX-induced SAH-A is associated with mitigated methyltransferase-activity, a one-of-a-kind report. Keywords: Metformin, Forskolin, Endothelial dysfunction, Methyltransferase, Cancer, Cardiovascular disease |
| Databáze: | OpenAIRE |
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