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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.

No MeSH data available.


Effect of MO on oxidative stress biomarkers, (A) serum TOC and (B) cardiac MDA and P.Carbonyl levels and (C) antioxidant enzyme activities in DOX-treated rats.Data are represented as mean ± S.E.M. of seven independent rats of each group. a P<0.05 vs. control; b P<0.05 vs. DOX.
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pone.0167049.g002: Effect of MO on oxidative stress biomarkers, (A) serum TOC and (B) cardiac MDA and P.Carbonyl levels and (C) antioxidant enzyme activities in DOX-treated rats.Data are represented as mean ± S.E.M. of seven independent rats of each group. a P<0.05 vs. control; b P<0.05 vs. DOX.

Mentions: Compared to control group significant elevation in serum TOC and cardiac levels of MDA and P.carbonyl was shown in DOX-intoxicated group (Fig 2A and 2B). The concurrent treatment with MO and DOX significantly attenuated the elevations of these oxidative stress biomarkers. This effect was dose dependent where higher doses of MO extract abolished DOX-induced oxidative stress evidently than the low dose. MO alone had no effect on TOC and MDA and P.carbonyl contents compared to the control group. Cardiac tissues of DOX-treated rats showed significant depletion in SOD activity (Fig 2C). The activity of CAT enzyme was, however, elevated significantly in heart tissues of that group. Nevertheless, treatment with medium and high doses of MO restored SOD activities in protected groups compared to DOX-treated one. No significant changes in the activities of either CAT or SOD were observed in rats treated with MO alone compared to control.


Melissa officinalis Protects against Doxorubicin-Induced Cardiotoxicity in Rats and Potentiates Its Anticancer Activity on MCF-7 Cells
Effect of MO on oxidative stress biomarkers, (A) serum TOC and (B) cardiac MDA and P.Carbonyl levels and (C) antioxidant enzyme activities in DOX-treated rats.Data are represented as mean ± S.E.M. of seven independent rats of each group. a P<0.05 vs. control; b P<0.05 vs. DOX.
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Related In: Results  -  Collection

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getmorefigures.php?uid=PMC5120835&req=5

pone.0167049.g002: Effect of MO on oxidative stress biomarkers, (A) serum TOC and (B) cardiac MDA and P.Carbonyl levels and (C) antioxidant enzyme activities in DOX-treated rats.Data are represented as mean ± S.E.M. of seven independent rats of each group. a P<0.05 vs. control; b P<0.05 vs. DOX.
Mentions: Compared to control group significant elevation in serum TOC and cardiac levels of MDA and P.carbonyl was shown in DOX-intoxicated group (Fig 2A and 2B). The concurrent treatment with MO and DOX significantly attenuated the elevations of these oxidative stress biomarkers. This effect was dose dependent where higher doses of MO extract abolished DOX-induced oxidative stress evidently than the low dose. MO alone had no effect on TOC and MDA and P.carbonyl contents compared to the control group. Cardiac tissues of DOX-treated rats showed significant depletion in SOD activity (Fig 2C). The activity of CAT enzyme was, however, elevated significantly in heart tissues of that group. Nevertheless, treatment with medium and high doses of MO restored SOD activities in protected groups compared to DOX-treated one. No significant changes in the activities of either CAT or SOD were observed in rats treated with MO alone compared to control.

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.