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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.


(A) ABTS, and (B) DPPH radical scavenging activities of MO ethanol extract and Trolox as reference antioxidant at various concentrations. (C) Representative HPLC phenolic acid profile of MO ethanol extract at 254 nm. Gallic acid (peak 1), caffeic acid (peak2), syringic acid (peak3), ferulic acid (peak4) and rosmarinic acid (peak 5). Values are means ± S.E.M. of three experiments.
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pone.0167049.g008: (A) ABTS, and (B) DPPH radical scavenging activities of MO ethanol extract and Trolox as reference antioxidant at various concentrations. (C) Representative HPLC phenolic acid profile of MO ethanol extract at 254 nm. Gallic acid (peak 1), caffeic acid (peak2), syringic acid (peak3), ferulic acid (peak4) and rosmarinic acid (peak 5). Values are means ± S.E.M. of three experiments.

Mentions: In the present investigation, the FRAP, ABTS and DPPH• were used to determine the antioxidant activities of MO extracts. The results of the three assays are summarized in Table 4. The FRAP assay is based on the reduction of oxidized ferric ions to ferrous ions by a given antioxidant. The reducing capacity of a given compound serves as a reliable indicator of its antioxidant potential. In this study, each gram of dried MO has high FRAP value, 0.48 mmol ascorbic acid equivalent. ABTS are other radical- scavenging methods that are broadly used to assess the ability of natural extracts to scavenge free radicals generated from those reagents. The MO exhibited high anti free radical scavenging activity where the ascorbic acid equivalent antioxidant capacities of the MO were 0.79±0.08 and 0.73±0.02 mmol/g in ABTS and DPPH assays, respectively. The ABTS and DPPH radical scavenging ability of samples (IC50) was 677.7± 0.39 and 743.6±1.29 μg/mL. The effect of MO was dose dependent (Fig 8A and 8B).


Melissa officinalis Protects against Doxorubicin-Induced Cardiotoxicity in Rats and Potentiates Its Anticancer Activity on MCF-7 Cells
(A) ABTS, and (B) DPPH radical scavenging activities of MO ethanol extract and Trolox as reference antioxidant at various concentrations. (C) Representative HPLC phenolic acid profile of MO ethanol extract at 254 nm. Gallic acid (peak 1), caffeic acid (peak2), syringic acid (peak3), ferulic acid (peak4) and rosmarinic acid (peak 5). Values are means ± S.E.M. of three experiments.
© Copyright Policy
Related In: Results  -  Collection

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

pone.0167049.g008: (A) ABTS, and (B) DPPH radical scavenging activities of MO ethanol extract and Trolox as reference antioxidant at various concentrations. (C) Representative HPLC phenolic acid profile of MO ethanol extract at 254 nm. Gallic acid (peak 1), caffeic acid (peak2), syringic acid (peak3), ferulic acid (peak4) and rosmarinic acid (peak 5). Values are means ± S.E.M. of three experiments.
Mentions: In the present investigation, the FRAP, ABTS and DPPH• were used to determine the antioxidant activities of MO extracts. The results of the three assays are summarized in Table 4. The FRAP assay is based on the reduction of oxidized ferric ions to ferrous ions by a given antioxidant. The reducing capacity of a given compound serves as a reliable indicator of its antioxidant potential. In this study, each gram of dried MO has high FRAP value, 0.48 mmol ascorbic acid equivalent. ABTS are other radical- scavenging methods that are broadly used to assess the ability of natural extracts to scavenge free radicals generated from those reagents. The MO exhibited high anti free radical scavenging activity where the ascorbic acid equivalent antioxidant capacities of the MO were 0.79±0.08 and 0.73±0.02 mmol/g in ABTS and DPPH assays, respectively. The ABTS and DPPH radical scavenging ability of samples (IC50) was 677.7± 0.39 and 743.6±1.29 μg/mL. The effect of MO was dose dependent (Fig 8A and 8B).

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.