Hesperidin as a preventive resistance agent in MCF–7 breast cancer cells line resistance to doxorubicin

Objective: To evaluate of hesperidin to overcome resistance of doxorubicin in MCF-7 resistant doxorubicin cells (MCF-7/Dox) in cytotoxicity apoptosis and P-glycoprotein (Pgp) expression in combination with doxorubicin. Methods: The cytotoxic properties, 50% inhibition concentration (IC50) and its co...

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Bibliographic Details
Main Authors: Rifki Febriansah, Dewi P.P. Dyaningtyas, Sarmoko, Nunuk Aries Nurulita, Edy Meiyanto, Agung Endro Nugroho
Format: Article
Language:English
Published: Wolters Kluwer Medknow Publications 2014-03-01
Series:Asian Pacific Journal of Tropical Biomedicine
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Online Access:http://www.sciencedirect.com/science/article/pii/S2221169115301970
Description
Summary:Objective: To evaluate of hesperidin to overcome resistance of doxorubicin in MCF-7 resistant doxorubicin cells (MCF-7/Dox) in cytotoxicity apoptosis and P-glycoprotein (Pgp) expression in combination with doxorubicin. Methods: The cytotoxic properties, 50% inhibition concentration (IC50) and its combination with doxorubicin in MCF-7 cell lines resistant to doxorubicin (MCF-7/Dox) cells were determined using MTT assay. Apoptosis induction was examined by double staining assay using ethidium bromide-acridine orange. Immunocytochemistry assay was performed to determine the level and localization of Pgp. Results: Single treatment of hesperidin showed cytotoxic activity on MCF-7/Dox cells with IC50 value of 11 μmol/L. Thus, combination treatment from hesperidin and doxorubicin showed addictive and antagonist effect (CI>1.0). Hesperidin did not increase the apoptotic induction, but decreased the Pgp expressions level when combined with doxorubicin in low concentration. Conclusions: Hesperidin has cytotoxic effect on MCF-7/Dox cells with IC50 of 11 μmol/L. Hesperidin did not increased the apoptotic induction combined with doxorubicin. Co-chemotherapy application of doxorubicin and hesperidin on MCF-7/Dox cells showed synergism effect through inhibition of Pgp expression.
ISSN:2221-1691