Antiproliferative effect of β-escin - an in vitro study

被引:20
作者
Mojzisova, Gabriela [1 ]
Kello, Martin [2 ]
Pilatova, Martina [2 ]
Tomeckova, Vladimira [3 ]
Vaskova, Janka [3 ]
Vasko, Ladislav [3 ]
Bernatova, Silvia [2 ]
Mirossay, Ladislav [2 ]
Mojzis, Jan [2 ]
机构
[1] Safarik Univ, Dept Expt Med, Fac Med, Kosice 04011, Slovakia
[2] Safarik Univ, Dept Pharmacol, Fac Med, Kosice 04011, Slovakia
[3] Safarik Univ, Dept Med & Clin Biochem, Fac Med, Kosice 04011, Slovakia
关键词
escin; apoptosis; mitochondria; fluorescence fingerprint; LUNG-CANCER CELLS; FACTOR-KAPPA-B; GLUTATHIONE-DEPLETION; OXIDATIVE STRESS; SEED EXTRACT; APOPTOSIS; PROLIFERATION; MITOCHONDRIA; FLUORESCENCE; TOXICITY;
D O I
10.18388/abp.2015_1013
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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.
引用
收藏
页码:79 / 87
页数:9
相关论文
共 58 条
[1]   Role of glutathione depletion and reactive oxygen species generation in apoptotic signaling in a human B lymphoma cell line [J].
Armstrong, JS ;
Steinauer, KK ;
Hornung, B ;
Irish, JM ;
Lecane, P ;
Birrell, GW ;
Peehl, DM ;
Knox, SJ .
CELL DEATH AND DIFFERENTIATION, 2002, 9 (03) :252-263
[2]   A1E inhibits proliferation and induces apoptosis in NCI-H460 lung cancer cells via extrinsic and intrinsic pathways [J].
Bak, Yesol ;
Ham, Sunyoung ;
Baatartsogt, O. ;
Jung, Seung Hyun ;
Choi, Kang-Duk ;
Han, Tae-Young ;
Han, Il-Young ;
Yoon, Do-Young .
MOLECULAR BIOLOGY REPORTS, 2013, 40 (07) :4507-4519
[3]  
Bombardelli E., 1996, Fitoterapia, V67, P483
[4]  
BRADFORD MM, 1976, ANAL BIOCHEM, V72, P248, DOI 10.1016/0003-2697(76)90527-3
[5]  
Calic-Dragosavac D., 2011, Advances in Environmental Biology, V5, P267
[6]   Escin reduces cell proliferation and induces apoptosis on glioma and lung adenocarcinoma cell lines [J].
Ciftci, Gulsen Akalin ;
Iscan, Arzu ;
Kutlu, Mehtap .
CYTOTECHNOLOGY, 2015, 67 (05) :893-904
[7]   Reactive oxygen species, cellular redox systems, and apoptosis [J].
Circu, Magdalena L. ;
Aw, Tak Yee .
FREE RADICAL BIOLOGY AND MEDICINE, 2010, 48 (06) :749-762
[8]   An integrated model of cardiac mitochondrial energy metabolism and calcium dynamics [J].
Cortassa, S ;
Aon, MA ;
Marbán, E ;
Winslow, RL ;
O'Rourke, B .
BIOPHYSICAL JOURNAL, 2003, 84 (04) :2734-2755
[9]   Free radicals antioxidant enzymes and lipid peroxidation in different types of leukemias [J].
Devi, GS ;
Prasad, MH ;
Saraswathi, I ;
Raghu, D ;
Rao, DN ;
Reddy, PP .
CLINICA CHIMICA ACTA, 2000, 293 (1-2) :53-62
[10]   Mitochondrial reactive oxygen species in cell death signaling [J].
Fleury, C ;
Mignotte, B ;
Vayssière, JL .
BIOCHIMIE, 2002, 84 (2-3) :131-141