ocotillol and Cardiomyopathies

Doxorubicin (Dox) has been clinically observed to exert marked anticancer activity. However, it is severely restricted by its associated dose‑dependent cardiotoxicity, which may be attenuated by decreasing the cumulative dosage via combining with a non‑toxic 'sensitizer'. We previously reported that ocotillol is capable of enhancing the antitumor activity of Dox; however, the effects of ocotillol on its cardiotoxicity remain unclear. In the current study, the effects of ocotillol on the toxicity of Dox were investigated, particularly its role in cardiotoxicity. In the acute injury model, pre‑administration of ocotillol prolonged the survival time. In the chronic animal model, pre‑administration of ocotillol decreased the elevated levels of plasma creatine kinase (CK) and CK‑MB, as well as attenuated the pathological changes that occurred. Pre‑treatment with ocotillol ameliorated the decreased glutathione level and reduced the cumulated malondialdehyde in the heart tissue. In addition, pre‑treatment with ocotillol restored the lowered white blood cell count. The results indicate that Dox co‑treatment with ocotillol may effectively alleviate its associated toxic injury, particularly cardiotoxicity. Thus, co‑administration of Dox with ocotillol may be a potential therapeutic strategy.

Topics: Acute Disease; Animals; Cardiomyopathies; Chronic Disease; Creatine Kinase, MB Form; Disease Models, Animal; Doxorubicin; Ginsenosides; Glutathione; Kaplan-Meier Estimate; Leukocyte Count; Leukocytes; Male; Malondialdehyde; Mice; Myocardium; Protective Agents

To investigate whether ocotillol, a derivate of pseudoginsenoside F11, might protect the heart against myocardial injury (MI) induced by isoproterenol (CAS 7683-59-2, ISO) in rats.. Male Sprague-Dawley rats were administered orally (5, 10 and 20 mg kg(-1)) for 8 days. During the last two days all animals except the normal control were administered ISO, 50 mg kg(-1) subcutaneously, for 2 consecutive days to induce myocardial injury. 8 h later, rats were anaesthetized and sacrificed. The biochemical parameters were assayed and pathological examination of the heart tissues was performed.. Ocotillol could significantly decrease the increased level of lactate dehydrogenase (LDH) in animals with myocardial injury induced by ISO. In the heart of ISO injected rats the superoxide dismutase (SOD) was decreased but the contents of malondialdehyde (MDA) were increased. Pre-treatment with ocotillol could attenuate the changes of both SOD and MDA. The ISO-induced pathohistological changes were also ameliorated by ocotillo.. The findings suggested that ocotillol could have cardioprotective effects on myocardial injury induced by ISO in rats, which may be, in part, by virtue of enhancing the antioxidative potency of the heart.

Topics: Adrenergic beta-Agonists; Animals; Antioxidants; Biomarkers; Cardiomyopathies; Cardiotonic Agents; Ginsenosides; Injections, Subcutaneous; Isoproterenol; L-Lactate Dehydrogenase; Male; Malondialdehyde; Myocardium; Rats; Rats, Sprague-Dawley; Superoxide Dismutase