期刊
ACTA BIOCHIMICA POLONICA
卷 63, 期 1, 页码 79-87出版社
ACTA BIOCHIMICA POLONICA
DOI: 10.18388/abp.2015_1013
关键词
escin; apoptosis; mitochondria; fluorescence fingerprint
资金
- Agency of the Slovak Ministry of Education for the Structural Funds of the EU [ITMS: 26220220104, ITMS: 26220120058, ITMS: 26220220152]
- Medicinsky univerzitny park v Kosiciach (MediPark, Kosice) - Operational Programme Research and Development [ITMS: 26220220185, OP VaV2012/2.2/08-RO, OPVaV/12/2013]
This study examined the antiproliferative effects of beta-escin (E) in cancer cells. The study showed that E inhibited cancer cells growth in a dose-dependent manner. The flow cytometric analysis revealed an escin-induced increase in the sub-G1 DNA content, which is considered to be a marker of apoptosis. Apoptosis was also confirmed by annexin V staining and DNA fragmentation assay. These effects were associated with increased generation of reactive oxygen species (ROS), caspase-3 activation and decreased mitochondrial membrane potential (MMP). Moreover, escin decreased mitochondrial protein content and mitochondrial fluorescence intensity as well as caused depletion of glutathione (GSH). However, activity of glutathione peroxidase (GPx) and glutathione reductase (GR) was not significantly changed in escin-treated cells. In conclusion, our results demonstrated that E has apoptotic effects in human cancer cells through the mechanisms involving mitochondrial perturbation. Although the exact mechanism needs to be investigated further, it can be concluded that E may be a useful candidate agent for cancer treatment.
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