Doxorubicin is a commonly used anticancer agent, which may cause cardiac toxicity. The present\nstudy designed to evaluate Phoenix dactylofera (dates) in doxorubicin (DXR) induced cardiac toxicity\nand cardiac remodeling in Wistar albino rats. The experimental rats procured, acclimatized\nand finally divided into five groups (n = 6). Group I served as normal controls, group II served as\ndisease controls and groups 3, 4 & 5 served as therapeutic groups (Phoenix dactylofera 5%, 10%,\nand 15% respectively). Cardiac remodeling and toxicity in the rats were induced by administration\nof DXR (1.25 mg/kg i.p. in 16 divided doses/month). At the end of protocol, effect of Phoenix\ndactylofera on cardiac remodeling was evaluated by measuring parameters like haemodynamics,\nheart weight, anatomy, Troponin T, creatine phosphokinase (CPK), creatine phosphokinase-MB\n(CPK-MB), Lactate dehydrogenase (LDH), serum glutamate oxaloacetate transaminase (SGOT),\nserum glutamate pyruvate transaminase (SGPT), calcium ion Ca2+, sodium ion Na+, potassium ion\nK+, intracellular enzymes like Malondialdehyde (MDA), glutathione (GSH), superoxide dismutase\n(SOD) and catalase (CAT). The disease control groups showed significantly elevated (p < 0.001)\nlevels of troponin T, CPK, CPK-MB, LDH, MDA, and significantly reduced levels (p < 0.001) of GSH,\nSOD & CAT while the levels of SGPT, SGOT were increased less significantly (p < 0.01) as compared\nto therapeutic groups. Treatment with Phoenix dactylofera significantly (p < 0.01) reduced the increased\nlevels of Troponin T, CPK, CPK-MB, LDH, SGOT, SGPT, MDA, GSH, SOD & CAT as well as restored\nCa2+, Na+, K+ levels to a normal value. Further, the histological studies of the cardiac tissues\ndemonstrated that the normal architecture of the cardiac cells was restored in the animals fed with dietary Phoenix dactylofera as compared to disease controls. The findings show that the administration\nof Phoenix dactylofera has the potential to prevent the toxicity induced by doxorubicin\nin the experimental rats.
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