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Oxidative Medicine and Cellular Longevity
Volume 2016, Article ID 6849758, 9 pages
Research Article

The Antiapoptosis Effect of Glycyrrhizate on HepG2 Cells Induced by Hydrogen Peroxide

Department of Pharmacology, Pharmacy School, Inner Mongolian Medical University, Jinshan Developing Zone, Hohhot, Inner Mongolia 010110, China

Received 17 April 2016; Revised 25 August 2016; Accepted 28 September 2016

Academic Editor: Javier Egea

Copyright © 2016 Miao Su et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


This study demonstrated that glycyrrhizate (GAS) could protect HEPG2 cells against damage and apoptosis induced by H2O2 (1600 μM, 4 h). Cell viability assay revealed that GAS was noncytotoxity at concentration 125 µg/mL, and GAS (5 μg/mL, 25 μg/mL, and 125 μg/mL) protected HepG2 cells against H2O2-induced cytotoxicity. H2O2 induced the HepG2 cells apoptosis, obvious morphologic changes were observed after Hochest 33258 staining, and more apoptotic cells were counted in flow cytometry assay compared to that of the natural group. Pretreatment GAS (5 μg/mL, 25 μg/mL, and 125 μg/mL) prior to H2O2 reverses the morphologic changes and reduced the apoptotic cells in HepG2 cells. GAS reduced the release of MDA, increased the activities of superoxide dismutase, and diminished the release of ALT and AST during oxidative stress in HepG2 cells. After Elisa kit detecting, GAS inhibited the caspase activity induced by H2O2, GAS decreased the level of caspase-3 and caspase-9 from mitochondria in dose-dependent manner. Western blot results showed that pretreatment GAS upregulated the expression of Bcl-2 and decreased the expression of Bax. These results reveal that GAS has the cytoprotection in HepG2 cells during ROS exposure by inhibiting the caspase activity in the mitochondria and influencing apoptogenic factors of the expression of Bax and Bcl-2.