Phoenix dactylifera Protects against Doxorubicin-Induced Cardiotoxicity and Nephrotoxicity

Doxorubicin (DOX) is an important anticancer drug used widely in the treatment of leukemia and lymphoma. The suitability of DOX is enhanced by its high therapeutic index, but its potential to cause cardiotoxicity and nephrotoxicity remains a prime concern in anticancer therapeutics. This study is de...

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Published inCardiology research and practice Vol. 2019; no. 2019; pp. 1 - 8
Main Authors Mehboob, Hania, Shi, Hailong, Ahmad, Fiaz ud Din, Chao, Xu, Wang, Yuewen, Hassan, Waseem
Format Journal Article
LanguageEnglish
Published Cairo, Egypt Hindawi Publishing Corporation 2019
Hindawi
John Wiley & Sons, Inc
Hindawi Limited
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Summary:Doxorubicin (DOX) is an important anticancer drug used widely in the treatment of leukemia and lymphoma. The suitability of DOX is enhanced by its high therapeutic index, but its potential to cause cardiotoxicity and nephrotoxicity remains a prime concern in anticancer therapeutics. This study is designed to determine the effect of Phoenix dactylifera extract (PDE) on DOX-induced cardiotoxicity and nephrotoxicity. Experimental rats were divided into four groups, receiving normal saline 4 ml/kg, DOX alone, and crude extract of PDE at doses of 1 g/kg and 1.5 g/kg in the presence of DOX, respectively, for 21 days. Cardiac enzymes and serum and urinary sodium and potassium levels were evaluated which were analyzed statistically by using one-way ANOVA. Subsequently, DOX initiated changes in the level of cardiac markers CK-MB, LDH, and troponin I, which were notably reversed by PDE. PDE was also effective against serum and urinary sodium and urinary potassium and protected against DOX-induced nephrotoxicity. Groups treated with different doses of PDE showed marked decrease in levels of cardiac and renal markers. The study concluded that the PDE extract possesses protective effects against DOX-induced cardiotoxicity and nephrotoxicity.
Bibliography:ObjectType-Article-1
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Academic Editor: Michael S. Wolin
ISSN:2090-8016
2090-0597
2090-0597
DOI:10.1155/2019/7395239