Cyanidin-3-glucoside prevents hydrogen peroxide (H 2 O 2 )-induced oxidative damage in HepG2 cells
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ORIGINAL RESEARCH PAPER
Cyanidin-3-glucoside prevents hydrogen peroxide (H2O2)induced oxidative damage in HepG2 cells Jiaqi Tan . Pengcheng Li . Hongkun Xue
. Qian Li
Received: 7 January 2020 / Accepted: 8 August 2020 Ó Springer Nature B.V. 2020
Abstract Objective The aim of this study is to evaluate the cytoprotection and potential molecular mechanisms of cyanidin-3-glucoside (C3G) on hydrogen peroxide (H2O2)-induced oxidative damage in HepG2 cells. Methods The 3-(4,5-dimethylthiazol-2-yl)-2,5diphenyltetrazolium bromide (MTT) assay was carried out to examine the viability of HepG2 cells exposure to H2O2 or C3G. Meanwhile, the antioxidant properties of C3G were measured by determining the activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase (CAT) and the Hong-Kun Xue and Qian Li are equally responsible for this study. J. Tan Academy for Advanced Interdisciplinary Studies, Peking University, No. 5 Yiheyuan Road, Haidian District, Beijing 100871, China P. Li H. Xue (&) Q. Li (&) Key Laboratory of Particle & Radiation Imaging, Ministry of Education, Department of Engineering Physics, Tsinghua University, No. 30 Shuangqing Road, Haidian District, Beijing 100084, China e-mail: [email protected] Q. Li e-mail: [email protected] P. Li College of Food Science and Technology, Jilin Agricultural University, No. 2888 Xincheng Street, Changchun 130118, Jilin, China
malondialdehyde (MDA) levels. Flow cytometry was employed to determine HepG2 cells apoptosis, and HepG2 cells were stained with Hoechst 33342 to observe cell morphology. 20 ,70 -dichlorofluorescin diacetate (DCFH-DA) was used to evaluate the production of intracellular reactive oxygen species (ROS). Finally, the expression of apoptosis-related protein was monitored through western blot analysis. Results HepG2 cells induced with H2O2 presented a remarkable decrease in cell viability that was suppressed when HepG2 cells were interfered with C3G (2.5–10 lM). C3G interference memorably and dosedependently inhibited H2O2-induced intracellular ROS and MDA overproduction, while C3G treatment markedly increased H2O2-induced the activities of intracellular SOD, GSH-Px and CAT. Eventually, the relative proteins expression levels of p53, cleaved caspase-9/3, cytochrome c, Fas-L, Fas, FADD and caspase-8 were substantially up-regulated in H2O2triggered HepG2 cells, and Bax/Bcl-2 ratio and the relative protein expression levels of PARP were dramatically down-regulated. However, the expression levels of these relative proteins were reversed in C3G-interfered HepG2 cells. Conclusions C3G could protect HepG2 cells from oxidative damage, and the effects that were mediated by the mitochondrial apoptotic pathways and the external pathways.
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Biotechnol Lett
Keywords Cyanidin-3-glucoside HepG2 cells Oxidative damage Apoptotic pathway
Introduction Oxidative damage is caused by excessive generation of reactive oxygen species (ROS) in terms of hydroxyl radicals, singlet oxygen and sup
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