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1.
Cancer Research and Clinic ; (6): 285-288, 2008.
Article in Chinese | WPRIM | ID: wpr-383840

ABSTRACT

Adriamycin is an effective and broad-spectrum anthracycline antineoplastic agent.However,long-term therapy with adriamycin is associated with a high incidence of cumulative and irreversible cardiomyopathy. Mechanisms about adriamycin-induced cardiotoxieity are complicated, including oxidative stress,mitochondrionopathy,cardiac apoptosis,and so on.For the past few years,a series of measures aye used,which attenuate the cardiotoxicity and uninfluence the antitumor effects.The review focuses on the mechanism and prevention of adriamycin-induced cardiotoxicity in order to improve the long term survival rate of neoplastic patient.

2.
Chinese Traditional and Herbal Drugs ; (24)1994.
Article in Chinese | WPRIM | ID: wpr-580055

ABSTRACT

Objective To investigate whether nobiletin could enhance chemotherapeutic drug-induced cell proliferation inhibition and apoptosis in breast carcinoma cells MDA-MB-231 in vitro.Methods MDA-MB-231 cells were exposed to nobiletin and different chemotherapeutic drugs at different concentration.The cell proliferation inhibitory rate was observed by MTT,apoptosis was detected by DNA Ladder,flow cytometry (FCM),and ELISA,and an NF-?B electrophoretic mobility shift was conducted by EMSA and ELISA.Results The combination of nobiletin (20 ?mol) with Taxol (1 nmol) or Doxorubicin (50 ng/mL) resulted in a significant inhibitory rate of cell growth and more apoptosis in MDA-MB-231 cells of 75.1% and 82.6% compared with either of them alone (40% and 45%),respectively.DNA Ladder and FCM assay showed that nobiletin could promote the cell apoptosis induced by chemotherapeutic drug.EMSA and ELISA assay showed that nobiletin could inhibit NF-?B activity in nuclear and cytoplasm of MDA-MB-231 cells.Conclusion The current results suggest that nobiletin could enhance the inhibition of chemotherapeutic drug on cell proliferation and cell apoptosis of breast carcinoma cells MDA-MB-231,the mechanism may be related to down-regulate the NF-?B activity in vitro.

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