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   Nov 26

Melissa officinalis Protects against Doxorubicin-Induced Cardiotoxicity in Rats and Potentiates Its Anticancer Activity on MCF-7 Cells

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Cardiotoxicity is a limiting factor of doxorubicin (DOX)-based anticancer therapy. Due to its beneficial effects, we investigated whether standardized extract of Melissa officinalis (MO) can attenuate doxorubicin-induced cardiotoxicity and can potentiate the efficacy of DOX against human breast cancer cells. MO was administered orally to male albino rats once daily for 10 consecutive days at doses of 250, 500 and 750 mg/kg b.wt. DOX (15 mg/kg b.wt. i.p.) was administered on the 8th day. MO protected against DOX-induced leakage of cardiac enzymes and histopathological changes. MO ameliorated DOX-induced oxidative stress as evidenced by decreasing lipid peroxidation, protein oxidation and total oxidant capacity depletion and by increasing antioxidant capacity. Additionally, MO pretreatment inhibited inflammatory responses to DOX by decreasing the expressions of nuclear factor kappa-B, tumor necrosis factor-alpha and cyclooxygenase-2 and the activity of myeloperoxidase. MO ameliorated DOX-induced apoptotic tissue damage in heart of rats. In vitro study showed that MO augmented the anticancer efficacy of DOX in human breast cancer cells (MCF-7) and potentiated oxidative damage and apoptosis. Thus, combination of DOX and MO may prove future cancer treatment protocols safer and more efficient.

Citation: Hamza AA, Ahmed MM, Elwey HM, Amin A (2016) Melissa officinalis Protects against Doxorubicin-Induced Cardiotoxicity in Rats and Potentiates Its Anticancer Activity on MCF-7 Cells. PLoS ONE 11(11): e0167049. doi:10.1371/journal.pone.0167049

Editor: Aamir Ahmad, University of South Alabama Mitchell Cancer Institute, UNITED STATES

Received: May 19, 2016; Accepted: November 8, 2016; Published: November 23, 2016

Copyright: © 2016 Hamza et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Data Availability: All relevant data are within the paper.

Funding: This work was supported by the Terry Fox Foundation, grant# 21S088. The funder had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

Competing interests: The authors have declared that no competing interests exist.

Abbreviations: ABTS, 2,2-azino-bis(3- ethylbenzothiazoline-6-sulfonate);AST, Aspartate aminotransferase;MDA, malondialdehyde;CAT, catalase;CK, Creatine kinase;CK-MB, CK isoenzyme-MB;COX-2, Cyclooxygenase-2;DOX, Doxorubicin;DPPH, 1,1-diphenyl-2-picrylhydrazyl;MPO, Myeloperoxidase;NF-kB, nuclear factor-kappa B;NO, nitric oxide;P.carbonyl, protein carbonyl;SOD, superoxide dismutase;TNF-α, Tumor necrosis alpha


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