| 人参皂苷对过氧化氢诱导的HepG2细胞损伤的保护作用 |
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| 引用本文： | 张聪,刘迪,张寒雪,张浩,孔繁利,冯宪敏. 人参皂苷对过氧化氢诱导的HepG2细胞损伤的保护作用[J]. 吉林大学学报(医学版), 2020, 46(5): 985-991. DOI: 10.13481/j.1671-587x.20200514 |
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| 作者姓名： | 张聪 刘迪 张寒雪 张浩 孔繁利 冯宪敏 |
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| 作者单位： | 1. 北华大学医学技术学院病理生理学教研室, 吉林 吉林 132013;2. 吉林医药学院基础医学院病原生物学教研室, 吉林 吉林 132013 |
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| 基金项目： | 吉林省卫计委卫生技术创新项目资助课题（2017J086）；吉林省卫计委中医药科技项目资助课题（2017083）；吉林省教育厅“十三五”科技项目资助课题（JJKH20180352KJ，JJKH20180354KJ）；吉林省吉林市科技创新发展计划项目资助课题（201831763）；北华大学研究生创新项目资助课题（〔2018〕039） |
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| 摘 要： | 目的：探讨人参皂苷对过氧化氢（H2O2）诱导的HepG2细胞氧化应激损伤的保护作用，并阐明其作用机制。方法：体外培养HepG2细胞，采用不同浓度（0.1、0.2、0.3、0.4、0.5、0.6、0.7、0.8和1.0 mmol·L-1）H2O2诱导HepG2细胞损伤。将HepG2细胞分为空白组、对照组、损伤组、人参皂苷对照组和人参皂苷保护组。10、20和40μmol·L-1人参皂苷RH1、F1、RD、RO和RE分别孵育细胞3 h，H2O2损伤2 h，采用细胞增殖与毒性检测试剂盒（CCK-8）检测细胞存活率，CAA法检测细胞抗氧化活性，2'，7'-二氯荧光黄双乙酸盐（DCFH-DA）荧光探针法检测细胞中活性氧（ROS）水平，WST-1法检测细胞中超氧化物歧化酶（SOD）活性。结果：H2O2半数抑制浓度（IC50）为0.4 mmol·L-1。与损伤组比较，10、20和40μmol·L-1人参皂苷RH1、F1、RD、RO和RE预处理后，H2O2诱导氧化损伤的HepG2细胞存活率均有不同程度的升高，其中人参皂苷F1保护组细胞存活率升高最明显（P<0.05）。与对照组比较，10、20和40μmol·L-1人参皂苷RH1、F1、RD、RO和RE保护组HepG2细胞存活率差异无统计学意义（P>0.05）。人参皂苷F1的半数效应浓度（EC50）为（15.82±0.82）μmol·L-1，CAA当量为（1 275.20±33.90）μmol TE/100 μmol·L-1人参皂苷F1。与对照组比较，损伤组细胞中ROS水平明显升高（P<0.05），SOD活性明显降低（P<0.05）；与损伤组比较，人参皂苷F1保护组细胞中ROS水平明显降低（P<0.05），SOD活性明显升高（P<0.05）。结论：人参皂苷F1通过提高细胞抗氧化能力，降低细胞中ROS水平，提高细胞SOD活性对H2O2诱导的HepG2细胞氧化应激损伤起到保护作用。
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| 关 键 词： | 人参皂苷 过氧化氢 HepG2细胞 氧化应激 氧自由基 |
| 收稿时间： | 2020-01-20 |
Protective effect of ginsenoside on hydrogen peroxide-induced HepG2 cell injury |
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| ZHANG Cong,LIU Di,ZHANG Hanxue,ZHANG Hao,KONG Fanli,FENG Xianmin. Protective effect of ginsenoside on hydrogen peroxide-induced HepG2 cell injury[J]. Journal of Jilin University: Med Ed, 2020, 46(5): 985-991. DOI: 10.13481/j.1671-587x.20200514 |
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| Authors: | ZHANG Cong LIU Di ZHANG Hanxue ZHANG Hao KONG Fanli FENG Xianmin |
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| Affiliation: | 1. Department of Pathophysiology, Academy of Medical Technology, Beihua University, Jilin 132013, China;2. Department of Pathogen Biology, School of Basic Medical Sciences, Jilin Medical University, Jilin 132013, China |
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| Abstract: | Objective: To explore the protective effect of ginsenoside on the oxidative stress injury of HepG2 cells induced by hydrogen peroxide(H2O2), and to clarify its mechanism. Methods: The HepG2 cells were cultured, and different concentrations (0.1, 0.2, 0.3, 0.4, 0.5, 0.6, 0.7, 0.8 and 1.0 mmol·L-1) of H2O2 were used to induce the HepG2 cell injury. The HepG2 cells were divided into blank group, control group, injury group, ginsenoside control group and ginsenoside protection group. The cells were incubated with 10,20 and 40 μmol·L-1 ginsenoside RH1, F1, RD, RO and RE for 3 h, and injured with H2O2 for 2 h; CCK-8 method was used to detect the cell survival rate, CAA method was used to detect the cell antioxidant capacity, DCFH-DA fluorescence probe method was used to detect the level of reactive oxygen species (ROS), and WST-1 method was used to detect the activity of superoxide dismutase (SOD). Results: The half inhibitory concentration (IC50) of H2O2 was 0.4 mmol·L-1. Compared with injury group, after 10, 20 and 40 μmol·L-1 ginsenoside RH1, F1, RD, RE and RO pretreatment, the survival rates of HepG2 cells induced by H2O2 were increased in varying degrees, and the cell survival rate in ginsenoside F1 protection group was most significantly increased (P<0.05). Compared with control group, in the survival rates of HepG2 cells in 10, 20 and 40 μmol·L-1 ginsenoside Rh1, F1, RD, and RO protection groups had no significant differences(P>0.05). The half effective concentration(EC50)of ginsenoside F1 was (15.82 ±0.82) μmol·L-1, and the CAA equivalent was (1275.20±33.90) μmol TE/100 μ mol·L-1 ginsenoside F1. Compared with control group, the ROS level in HepG2 cells in injury group was significantly increased (P<0.05) and the SOD activity was significantly decreased (P<0.05). Compared with injury group, the ROS level in HepG2 cells in ginsenoside F1 protection group was significantly decreased (P<0.05) and the SOD activity was significantly increased (P<0.05). Conclusion: Ginsenoside F1 can protect the stress injury of HepG2 cells induced by H2O2 by the increasing the cell antioxidant capacity, decreasing the ROS level and increasing the SOD activity. |
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| Keywords: | ginsenoside hydrogen peroxide HepG2 cells oxidative stress reactive oxygen species |
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