Protection against doxorubicin cardiomyopathy in rats: role of phosphodiesterase inhibitors type 4

The Journal of Pharmacy and Pharmacology
Hoda E MohamedTamer M Abd el-Fattah

Abstract

Selective cardiotoxicity of doxorubicin (DOX) remains a significant and dose-limiting clinical problem. The mechanisms implicated are not yet fully defined but may involve the production of reactive oxygen species or expression of cytokines. Although patients with advanced congestive heart failure express elevated circulating levels of tumour necrosis factor-alpha (TNFalpha), little is known about the prognostic importance and regulation of TNF in the heart in cardiac disease states. Here we tested whether the expression of TNFalpha, along with oxidative stress, is associated with the development of DOX-induced cardiomyopathy (DOX-CM) and whether concurrent treatment with taurine (Taur), an antioxidant, or rolipram (Rolp), a TNFalpha inhibitor, offer a certain protection against DOX cardiotoxic properties. DOX (cumulative dose, 12 mg kg(-1)) was administered to rats in six equal (intraperitoneal) injections over a period of 6 weeks. Cardiomyopathy was evident by myocardial cell damage, which was characterized by a dense indented nucleus with peripheral heterochromatin condensation and distorted mitochondria, as well as significant increase in serum levels of creatine kinase and lactate dehydrogenase. DOX also induced an increme...Continue Reading

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