Journal
MOLECULAR MEDICINE REPORTS
Volume 13, Issue 5, Pages 3953-3960Publisher
SPANDIDOS PUBL LTD
DOI: 10.3892/mmr.2016.5017
Keywords
doxorubicin; berberine; hepatorenal toxicity; oxidative damage
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Funding
- Natural Science Foundation of China [81273600, 81302773]
- natural science Foundation of Hebei Province [C2011206145, H2013206147]
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Doxorubicin (DOX), a potent broad-spectrum chemotherapeutic agent used for the treatment of several types of cancer, is largely limited due to its serious side effects on non-target organs. Thus, the present study aimed to investigate whether berberine (Ber), an isoquinoline alkaloid, could reduce DOX-induced acute hepatorenal toxicity in rats. Fifty rats were randomly divided into five groups: i) Control group, ii) DOX group, iii) DOX+Ber (5 mg kg) group; iv) DOX+Ber (10 mg kg), and v) DOX+Ber (20 mg kg) group. In the tests, body weight, organ index, general condition and mortality were observed. In addition, the serum levels of alanine transaminase (ALT), aspartate aminotransferase (AST), total cholesterol (TCHO) and blood urea nitrogen (BUN) were determined to evaluate hepatorenal function. Hepatorenal toxicity was further assessed using hematoxylin and eosin stained sections. Furthermore, the levels of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and malondialdehyde (MDA) in rat serum or tissue homogenate were also assessed to determine the mechanisms of action. Results suggested that pretreatment with Ber ameliorated the DOX-induced liver and kidney injury by lowering the serum ALT, AST, TCHO and BUN levels, and the damage observed histologically, such as hemorrhage and focal necrosis of liver and kidney tissues induced by DOX were also attenuated by Ber. Furthermore, Ber also exerted certain antioxidative properties through reversing the changes in the levels of MDA, SOD, GSH and MDA induced by DOX. These findings indicate that Ber has protective effects against DOX-induced acute hepatorenal toxicity in rats. Combination of Ber with DOX is a novel strategy that has the potential for protecting against DOX-induced hepatorenal toxicity in clinical practice.
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