Influence of p-coumaric acid on doxorubicin-induced oxidative stress in rat's heart

被引:145
作者
Abdel-Wahab, MH
El-Mahdy, MA
Abd-Ellah, MF
Helal, GK
Khalifa, F
Hamada, FMA
机构
[1] Al Azhar Univ, Fac Pharm, Dept Pharmacol & Toxicol, Cairo, Egypt
[2] Univ Kostantine, Fac Sci, Dept Biol, Kostantine, Algeria
关键词
rat; cardiotoxicity; doxorubicin; oxidative stress; antioxidants; phenolic acids; p-coumaric acid; INDUCED CARDIOTOXICITY; ANTHRACYCLINE ANTIBIOTICS; ADRIAMYCIN CARDIOMYOPATHY; LIPID-PEROXIDATION; HYDROGEN-PEROXIDE; CARDIAC TOXICITY; PREVENTION; THYMOQUINONE; MOUSE; GLUTATHIONE;
D O I
10.1016/S1043-6618(03)00214-7
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
The therapeutic value of doxorubicin (DOX) as anticancer antibiotic is limited by its cardiotoxicity. The implication of natural phenolic acids in the prevention of many pathologic diseases has been reported. Herein, the ability of p-coumaric (PC) acid, a member of phenolic acids, to protect rat's heart against DOX-induced oxidative stress was investigated. Three main groups of albino rats were used; DOX, PC, and PC plus DOX-receiving animals. Corresponding control animals were also used. DOX was administered i.p. in a single dose of 15 mg kg(-1). PC alone, in a dose of 100 mg kg(-1), was orally administered for five consecutive days. In PC/DOX group, rats received PC 5 days prior to DOX. DOX-induced high serum levels of lactic dehydrogenase (LDH) and creatine phosphokinase (CPK), were reduced significantly by PC administration, compared to DOX-receiving rats. Pretreatment with PC ameliorated the cardiac content of glutathione (GSH), and superoxide dismutase (SOD) & catalase (CAT) activities, compared to DOX-receiving rats. On the other hand, accumulation of cardiac content of MDA significantly decreased following PC pretreatment, compared to DOX-treated rats. The data presented here indicate that PC protects rats hearts against DOX-induced oxidative stress in the heart. It may be worthy to consider the usefulness of PC as adjuvant therapy in cancer management. (C) 2003 Elsevier Ltd. All rights reserved.
引用
收藏
页码:461 / 465
页数:5
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