What is it about?
. 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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Why is it important?
Our study provides evidences for 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 heartMO may be beneficial for DOX-induced cardiotoxicity. This, however, needs to be confirmed in a more clinically relevant model to elucidate the mechanism and develop strategies in prevention against DOX-induced cardiotoxicity.
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This page is a summary of: Melissa officinalis Protects against Doxorubicin-Induced Cardiotoxicity in Rats and Potentiates Its Anticancer Activity on MCF-7 Cells, PLoS ONE, November 2016, PLOS,
DOI: 10.1371/journal.pone.0167049.
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