title: The Antiapoptosis Effect of Glycyrrhizate on HepG2 Cells Induced by Hydrogen Peroxide.
abstract: This study demonstrated that glycyrrhizate (GAS) could protect HEPG2 cells against damage and apoptosis induced by H2O2(1600μM, 4 h). Cell viability assay revealed that GAS was noncytotoxity at concentration 125µg/mL, and GAS (5μg/mL, 25μg/mL, and 125μg/mL) protected HepG2 cells against H2O2-induced cytotoxicity. H2O2induced 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 (5μg/mL, 25μg/mL, and 125μg/mL) prior to H2O2reverses 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.
authors.affiliation: Department of Pharmacology, Pharmacy School, Inner Mongolian Medical University, Jinshan Developing Zone, Hohhot, Inner Mongolia 010110, China.
authors.forename: Miao
authors.initials: M
authors.lastname: Su
authors.affiliation: Department of Pharmacology, Pharmacy School, Inner Mongolian Medical University, Jinshan Developing Zone, Hohhot, Inner Mongolia 010110, China.
authors.forename: Tengfei
authors.initials: T
authors.lastname: Yu
authors.affiliation: Department of Pharmacology, Pharmacy School, Inner Mongolian Medical University, Jinshan Developing Zone, Hohhot, Inner Mongolia 010110, China.
authors.forename: Hong
authors.initials: H
authors.lastname: Zhang
authors.affiliation: Department of Pharmacology, Pharmacy School, Inner Mongolian Medical University, Jinshan Developing Zone, Hohhot, Inner Mongolia 010110, China.
authors.forename: Yan
authors.initials: Y
authors.lastname: Wu
authors.affiliation: Department of Pharmacology, Pharmacy School, Inner Mongolian Medical University, Jinshan Developing Zone, Hohhot, Inner Mongolia 010110, China.
authors.forename: Xiaoqin
authors.initials: X
authors.lastname: Wang
authors.affiliation: Department of Pharmacology, Pharmacy School, Inner Mongolian Medical University, Jinshan Developing Zone, Hohhot, Inner Mongolia 010110, China.
authors.forename: Gang
authors.identifier: 0000-0002-0368-7528
authors.initials: G
authors.lastname: Li
mesh_terms: D000410:Alanine Transaminase / Q000378:metabolism; D017209:Apoptosis / Q000187:drug effects*; D001219:Aspartate Aminotransferases / Q000378:metabolism; D006690:Bisbenzimidazole / Q000378:metabolism; D020169:Caspases / Q000378:metabolism; D004789:Enzyme Activation / Q000187:drug effects; D019695:Glycyrrhizic Acid / Q000494:pharmacology*; D056945:Hep G2 Cells; D006801:Humans; D006861:Hydrogen Peroxide / Q000633:toxicity*; D015227:Lipid Peroxidation / Q000187:drug effects; D008315:Malondialdehyde / Q000378:metabolism; D013194:Staining and Labeling; D013482:Superoxide Dismutase / Q000378:metabolism; D051028:bcl-2-Associated X Protein / Q000378:metabolism
chemical_list: D051028:bcl-2-Associated X Protein; D008315:Malondialdehyde; D019695:Glycyrrhizic Acid; D006861:Hydrogen Peroxide; D013482:Superoxide Dismutase; D001219:Aspartate Aminotransferases; D000410:Alanine Transaminase; D020169:Caspases; D006690:Bisbenzimidazole