Ameliorative effect of propolis against cyclophosphamide-induced toxicity in mice
Authors:
- Sabry A. El-NaggarSESabry A. El-Naggar
- Abeer A. Alm-EldeenAAAbeer A. Alm-Eldeen
- Mousa O. GermoushMGMousa O. Germoush
- Kamal F. El-BorayKEKamal F. El-Boray
- Hassan A. ElgebalyHEHassan A. Elgebaly
- 7 October 2014
- journal article
- Published by Taylor & Francis in Pharmaceutical Biology
- Vol. 53 (2) , 235-241
Abstract
Cyclophosphamide (CTX) is a common anticancer agent used for the treatment of several malignancies. However, upon treatment, it induces severe toxicity due to its oxidative stress capability. Propolis, a natural product collected by honey bees, has shown several biological activities, such as free radical scavenging and antioxidant agent. This study elucidates the protective effects of propolis against CTX-induced changes in mice. Forty-eight male Swiss albino mice were divided into four groups; group 1 was intraperitoneally (i.p.) injected with 200 µL of phosphate buffer saline (PBS), group 2 was injected with 100 mg/kg/d propolis, group 3 was injected with a single dose of CTX (200 mg/kg), and group 4 was injected with a single dose of CTX (200 mg/kg) followed by propolis (100 mg/kg) for 7 consecutive days. After 12 d, mice were bled and then sacrificed to analyze the hematological, biochemical, and histological parameters. The results indicated that CTX-injected mice showed an increase in the levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), urea, and creatinine and a decrease in the total number of white blood cells (WBCs) and platelets. Moreover, dramatically changes in the histological architectures of the liver and kidney were observed. The mice that were injected with CTX/propolis showed an improvement in the levels of ALT, AST, urea, creatinine, WBCs, and platelets. Moreover, the histological picture of the liver and kidney was significantly improved. In conclusion, propolis might be considered an effective agent in ameliorating the toxicity resulted from CTX treatment.Keywords
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