POTENTIAL PROTECTIVE EFFECT OF GUM ARABIC AGAINST DOXORUBICIN-INDUCED CARDIOTOXICITY IN WISTAR ALBINO RATS

Gum Arabic (GA) is a water-soluble polysaccharide, obtained from stems of Acacia senegal trees as gummy exudates and it is metabolized in colon by normal flora into volatile fatty acids. It is a beneficial adjunct to the low-protein diet for chronic renal failure patient because it reduces serum urea nitrogen level. It increases water and electrolyte absorption, so that it could be a good additive to the oral rehydration solutions, in patient suffering from diarrhea. It is also have a good protective activity against CCl4 and acetaminophen-induced hepatotoxicity in rats but it failed protect kidney from gentamicin-induced nephrotoxicity. The goal of current study was to investigate the cardioprotective of gum arabic aqueous extract against cardiotoxicity induced by doxorubicin in rats. Wistar albino rats were divided into four groups, 5 rats in each group: Group A (distilled water only, as a control), group B (Doxorubicin (DOX)-only treated rats, 15mg/Kg, IP as a single loading dose), group C (GA 10g/Kg body weight, orally for 4weeks prior DOX treatment) and Group D (GA-only treated group). Histopathological examination and serum biomarker enzymes like Creatine Kinase (CK), Lactate Dehydrogenase (LDH), serum aspartate transaminase (AST) and serum alanine transaminase (ALT) level were monitored at the end of study to evaluate cardiotoxicity. The study showed that doxorubicin-treated animals increased the levels of CK, LDH and ALT significantly and gum arabic-pretreated rats decreased the level of LDH significantly. In gum arabic-only treated animals, they showed no significant changes in all the serum enzymes compared with the control group. Histopathological studies of the heart showed marked cardiac muscle damage in doxorubicin treated rats and the damage was less in gum arabic treated rats prior doxorubicin administration. The results indicate that gum arabic administration have potential protective effect against doxorubicin-induced cardiotoxicity.