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Molecules 2016, 21(7), 872; doi:10.3390/molecules21070872

18α-Glycyrrhetinic Acid Induces Apoptosis of HL-60 Human Leukemia Cells through Caspases- and Mitochondria-Dependent Signaling Pathways

1
Department of Biological Science and Technology, China Medical University, Taichung 404, Taiwan
2
Department of Chinese Pharmaceutical Sciences and Chinese Medicine Resources, China Medical University, Taichung 404, Taiwan
3
College of Chinese Medicine, School of Post-Baccalaureate Chinese Medicine, China Medical University, Taichung 404, Taiwan
4
Division of Cardiology, China Medical University Hospital, Taichung 404, Taiwan
5
Department of Anesthesiology, China Medical University Hospital, Taichung 404, Taiwan
6
Department of Medicine, China Medical University, Taichung 404, Taiwan
7
School of Pharmacy, China Medical University, Taichung 404, Taiwan
8
Department of Biotechnology, Asia University, Taichung 413, Taiwan
These authors contributed equally to this work.
*
Authors to whom correspondence should be addressed.
Academic Editor: Derek J. McPhee
Received: 18 May 2016 / Revised: 21 June 2016 / Accepted: 25 June 2016 / Published: 1 July 2016
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Abstract

In this study we investigate the molecular mechanisms of caspases and mitochondria in the extrinsic and intrinsic signal apoptosis pathways in human leukemia HL-60 cells after in vitro exposure to 18α-glycyrrhetinic acid (18α-GA). Cells were exposed to 18α-GA at various concentrations for various time periods and were harvested for flow cytometry total viable cell and apoptotic cell death measurements. Cells treated with 18α-GA significantly inhibited cell proliferation and induced cell apoptosis in a dose-dependent manner, with an IC50 value of 100 μM at 48 h. The cell growth inhibition resulted in induction of apoptosis and decreased the mitochondria membrane potential (ΔΨm) and increased caspase-8, -9 and -3 activities. Furthermore, cytochrome c and AIF were released from mitochondria, as shown by western blotting and confirmed by confocal laser microscopy. Western blotting showed that 18α-GA increased the levels of pro-apoptotic proteins such as Bax and Bid and decreased the anti-apoptotic proteins such as Bcl-2 and Bcl-xl, furthermore, results also showed that 18α-GA increased Fas and Fas-L which are associated with surface death receptor in HL-60 cells. Based on those observations, the present study supports the hypothesis that 18α-GA-induced apoptosis in HL-60 cells involves the activation of the both extrinsic and intrinsic apoptotic pathways. View Full-Text
Keywords: 18α-glycyrrhetinic acid; mitochondria; caspase-3; apoptosis; HL-60 cells 18α-glycyrrhetinic acid; mitochondria; caspase-3; apoptosis; HL-60 cells
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MDPI and ACS Style

Huang, Y.-C.; Kuo, C.-L.; Lu, K.-W.; Lin, J.-J.; Yang, J.-L.; Wu, R.S.-C.; Wu, P.-P.; Chung, J.-G. 18α-Glycyrrhetinic Acid Induces Apoptosis of HL-60 Human Leukemia Cells through Caspases- and Mitochondria-Dependent Signaling Pathways. Molecules 2016, 21, 872.

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