Abstract
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.
Highlights
Doxorubicin (DOX) belongs to class of anthracyclines isolated from bacteria Streptomyces peucetius in the early 1960s
Elevated levels of serum concentration of different cardiac biomarkers such as CK-MB (Figure 1(a)), LDH (Figure 1(b)), and troponin I (Figure 1(c)) showed quantitative index of myocardial damage induced by DOX compared with the normal control group, and values were markedly lowered in groups treated with DOX
Level of serum sodium was increased in group treated with DOX at a single dose of 10 mg/kg compared with the normal control group, while there is notable reduction in sodium level in groups treated with Phoenix dactylifera extract (PDE) at a dose of 1 g/kg and 1.5 g/kg (Figure 2(a))
Summary
Doxorubicin (DOX) belongs to class of anthracyclines isolated from bacteria Streptomyces peucetius in the early 1960s. Pathogenesis of DOX-induced cardiomyopathy is implicated by multiple mechanisms including oxidative stress, downregulation of functional cardiac muscle-specific and mitochondrial proteins, inhibition and activation of enzymatic pathways, and exaggerated immune response. All these pathological events lead to Cardiology Research and Practice altered molecular signaling and activation of apoptotic cascade resulting in the destruction of nucleic acid, sarcomere disruption, and myofibril loss [8]. In view of its anticancer, antioxidant effects and effects against various toxicities, we attempted to examine the effects of date palm fruit extracts on DOX-induced cardiotoxicity and nephrotoxicity, which is one of the prevalent problems in the clinical use of DOX
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