Antiproliferative effect of β-escin - an in vitro study.

Gabriela Mojžišová; Martin Kello; Martina Pilátová; Vladimíra Tomečková; Janka Vašková; Ladislav Vaško; Silvia Bernátová; Ladislav Mirossay; Ján Mojžiš

doi:10.18388/abp.2015_1013

Gabriela Mojžišová Department of Experimental Medicine, Faculty of Medicine, P. J. Šafárik University, 040 11 Košice, Slovak Republic.;
Martin Kello Department of Pharmacology, Faculty of Medicine, P. J. Šafárik University, 040 11 Košice, Slovak Republic.;
Martina Pilátová Department of Pharmacology, Faculty of Medicine, P. J. Šafárik University, 040 11 Košice, Slovak Republic.;
Vladimíra Tomečková Department of Medical and Clinical Biochemistry, Faculty of Medicine, P. J. Šafárik University, 040 11 Košice, Slovak Republic.;
Janka Vašková Department of Medical and Clinical Biochemistry, Faculty of Medicine, P. J. Šafárik University, 040 11 Košice, Slovak Republic.;
Ladislav Vaško Department of Medical and Clinical Biochemistry, Faculty of Medicine, P. J. Šafárik University, 040 11 Košice, Slovak Republic.;
Silvia Bernátová Department of Pharmacology, Faculty of Medicine, P. J. Šafárik University, 040 11 Košice, Slovak Republic.;
Ladislav Mirossay Department of Pharmacology, Faculty of Medicine, P. J. Šafárik University, 040 11 Košice, Slovak Republic.;
Ján Mojžiš Department of Pharmacology, Faculty of Medicine, P. J. Šafárik University, 040 11 Košice, Slovak Republic.;

DOI: https://doi.org/10.18388/abp.2015_1013

Abstract

This study examined the antiproliferative effects of β-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.