COMPARATIVE STUDY
JOURNAL ARTICLE

Cardioprotective activity of standardized extract of Ficus racemosa stem bark against doxorubicin-induced toxicity

Faiyaz Ahmed, Asna Urooj
Pharmaceutical Biology 2012, 50 (4): 468-73
22136326

CONTEXT: Ficus racemosa Linn. (Moraceae) bark is a rich source of phenolic compounds having diverse biological properties including antioxidant activity. The present study evaluated the cardioprotective activity of sequential acetone extract of Ficus racemosa bark against doxorubicin-induced cardiotoxicity in rats.

MATERIALS AND METHODS: The extract was standardized by high-performance liquid chromatography (HPLC) and subjected to acute toxicological evaluation in mice. Cardiotoxicity was induced by administration of doxorubicin (10 mg kg(-1) i.v.) to the extract pretreated rats (250 and 500 mg kg(-1)) and compared with that of Arjuna, a standard cardiotonic. Biochemical parameters included CK-MB, LDH, AST, ALT, troponin I, thiobarbituric acid reactive substances (TBARS), and glutathione.

RESULTS: The HPLC fingerprinting of the extract indicated the presence of bergenin (0.89%) and bergapten (0.07%). In an acute toxicity study, the extract at a dose of 2 g kg(-1) did not cause any adverse changes and no mortality was observed. Administration of doxorubicin significantly increased (p ≤ 0.05) serum levels of creatine kinase, lactate dehydrogenase, aspartate aminotransferase, and alanine aminotransferase, which were decreased to an extent of 68, 63, 41, and 65%, respectively, in extract pretreated group (500 mg kg(-1)). Troponin I was undetected in control group, while it was found in serum of all the experimental groups. The extract pretreatment significantly decreased (p ≤ 0.05) TBARS and increased glutathione levels in serum and cardiac tissue. These observations were further substantiated by the histopathological studies.

CONCLUSION: The acetone extract of F. racemosa bark possesses potential cardioprotective activity against doxorubicin-induced cardiotoxicity in rats by scavenging free radicals generated by the administration of the drug.

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