期刊
BIOCHEMICAL PHARMACOLOGY
卷 71, 期 5, 页码 584-595出版社
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.bcp.2005.11.026
关键词
apoptosis; doxorubicin; schisandrin B; caspase; cardiomyocytes
The dose-dependent cardiotoxicities of doxorubicin (DOX) significantly limits its anticancer efficacies. One of the ways to augment the efficacies of DOX at a relatively low cumulative dose is to use a chemical sensitizer. Here, we demonstrated that schisandrin B (Sch B) significantly enhanced DOX-induced apoptosis of SMMC7721, a human hepatic carcinoma cell line, and of MCF-7, a human breast cancer cell line. This enhancement was irrelevant to the action of Sch B on P-glycoprotein or other drug-transporters, but associated with the activation of caspase-9 rather than caspase-8. The loss of mitochondria membrane potential was observed when cells were treated with DOX and Sch B combined. On the other hand, at the same experimental conditions, Sch B did not enhance the DOX-induced apoptosis of primary rat cardiomyocytes and primary human fibroblasts. Therefore, it is speculative that Sch B may bring benefit to clinical chemotherapy by reducing significantly the cumulative doses of DOX and its associated cardiotoxicities. (c) 2005 Elsevier Inc. All rights reserved.
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