Terminalia chebula Retz: A Prospective Agent in Reducing the Doxorubicin‑Mediated Cardiotoxicity

ABSTRACT

Objectives: The present study evaluated the role of Terminalia chebulaRetz. extract against doxorubicin (DXR)‑mediated cardiac damages in male and female rats.Materials and Methods: The ethanolic extract of T. chebula (0.25, 0.5, and 1 g/kg) was administered simultaneously with DXR (2.5 mg/kg, three‑doses on alternate days by intraperitoneal route). Two additional groups were evaluated by administering 0.5 g/kg of the extract to animals before or after DXR treatment. The study was done separately in male and female adult Wistar rats of bodyweight 180–200 mg. The cardiac biomarker levels such as creatine kinase‑monoenzyme B, lactate dehydrogenase, alanine aminotransferase, and aspartate aminotransferase were estimated after each treatment. Histopathology of cardiac tissue was studies analyzed, and the level of superoxide dismutase was determined in serum. The results were statistically analyzed using one‑way ANOVA and Bonferroni tests and P < 0.05 was considered to indicate the statistical significance. Results:The observations indicated that DXR significantly (P< 0.001) elevated the biomarker levels of cardiac damage in both male and female rats, besides inducing the structural changes in the myocardium tissues and antioxidant status. The co‑administration of higher doses ofT. chebula extract (0.5 and 1 g/kg) with DXR significantly (P < 0.01) reduced the cardiac enzyme levels and histopathological changes and improve the antioxidant status compared to DXR group. Post-treatment with T. chebula(0.5 mg/kg) showed mild inhibitory action on the DXR‑induced cardiac changes without significantly affecting the antioxidant level. Conclusion:The results suggest that co‑administration of T. chebulareduced the DXR‑mediated cardiac damages and the action could be related to the enhancement of the antioxidant property in rats.

KEYWORDS

• Cardiac biomarkers
• Doxorubicin
• Oxidative stress
• Terminalia chebula

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• DOI10.4103/pr.pr_109_19Copy

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