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Melissa officinalis Protects 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 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.

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MO blocks DOX-induced apoptosis, -ROS formation and –necrosis and down regulates the induced inflammation in vivo.In human breast cancer cells (MCF-7), MO improves the anticancer efficacy of DOX and potentiates oxidative damage and apoptosis.
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pone.0167049.g009: MO blocks DOX-induced apoptosis, -ROS formation and –necrosis and down regulates the induced inflammation in vivo.In human breast cancer cells (MCF-7), MO improves the anticancer efficacy of DOX and potentiates oxidative damage and apoptosis.

Mentions: The present study substantiates the promising ameliorating effects of MO against DOX-induced cardiotoxicity in rats through modulation of oxidative stress, diminution of inflammation and abrogation of apoptosis in rat heart (Fig 9). Identification of a mechanism for MO anticancer effect introduces the possibility that combining this plant with DOX might enhance the therapeutic efficacy of DOX in clinical oncology. Beneficial effect of the MO extract is likely due to the synergistic interactions of phenolic compounds and other triterpene acids of MO. Accordingly, this study provides new insights into the development of strategies to augment anticancer activity of DOX and further to alleviate its cardiotoxicity. Further confirmatory studies both at preclinical and clinical levels are needs to evaluate a combination therapy.


Melissa officinalis Protects against Doxorubicin-Induced Cardiotoxicity in Rats and Potentiates Its Anticancer Activity on MCF-7 Cells
MO blocks DOX-induced apoptosis, -ROS formation and –necrosis and down regulates the induced inflammation in vivo.In human breast cancer cells (MCF-7), MO improves the anticancer efficacy of DOX and potentiates oxidative damage and apoptosis.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC5120835&req=5

pone.0167049.g009: MO blocks DOX-induced apoptosis, -ROS formation and –necrosis and down regulates the induced inflammation in vivo.In human breast cancer cells (MCF-7), MO improves the anticancer efficacy of DOX and potentiates oxidative damage and apoptosis.
Mentions: The present study substantiates the promising ameliorating effects of MO against DOX-induced cardiotoxicity in rats through modulation of oxidative stress, diminution of inflammation and abrogation of apoptosis in rat heart (Fig 9). Identification of a mechanism for MO anticancer effect introduces the possibility that combining this plant with DOX might enhance the therapeutic efficacy of DOX in clinical oncology. Beneficial effect of the MO extract is likely due to the synergistic interactions of phenolic compounds and other triterpene acids of MO. Accordingly, this study provides new insights into the development of strategies to augment anticancer activity of DOX and further to alleviate its cardiotoxicity. Further confirmatory studies both at preclinical and clinical levels are needs to evaluate a combination therapy.

View Article: PubMed Central - PubMed

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 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.

No MeSH data available.


Related in: MedlinePlus