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

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Abstract

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 dosages 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 witnessed by decreasing lipid peroxidation, protein oxidation and total oxidant capability depletion and by increasing antioxidant capability. Additionally, MO pretreatment impeded 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 injury in heart of rats. In vitro examine showed that MO augmented the anticancer efficacy of DOX in human breast cancer cells( MCF-7) and potentiated oxidative injury and apoptosis. Thus, combining of DOX and MO may demonstrate future cancer therapy 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

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

Copyright: A( c) 2016 Hamza et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted employ, distribution, and reproduction in any medium, the original writer and source are credited.

Data Availability: All relevant data are within the paper.

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

Competing interests: The authors have declared that no vying 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 ;D OX, Doxorubicin ;D PPH, 1,1 -diphenyl-2-picrylhydrazyl; MPO, Myeloperoxidase; NF-kB, nuclear factor-kappa B; NO, nitric oxide ;P. carbonyl, protein carbonyl; SOD, superoxide dismutase; TNF-I +-, Tumor necrosis alpha

Source: PLOSONE

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