人参皂苷Rg1对氟化钠致肝L-02细胞线粒体氧化应激损伤的保护作用

The Protective Effects of Ginsenoside Rg1 on Mitochondrial Oxidative Stress L02 Hepatocytes Induced by Sodium Fluoride

目的:探讨人参皂苷Rg1(G-Rg1)对氟化钠引起的肝L-02细胞线粒体氧化损伤的保护作用。方法:体外培养肝L-02细胞,4mM氟化钠染毒24 h,同时给予20 ng/mL、40 ng/mL、80 ng/mL的G-Rg1干预。DCFH-DA荧光探针检测细胞内ROS含量;JC-1荧光探针检测细胞线粒体膜电位变化;Elisa法检测细胞内8-OHdG含量;单细胞凝胶电泳技术检测细胞DNA的损伤情况;同时检测细胞内MDA、GSH含量变化。结果:与正常对照组相比,氟化钠染毒组细胞内ROS及8-OHdG水平明显增高,线粒体膜电位下降,细胞拖尾率、尾长和Olive尾矩显著升高,MDA含量明显增高,GSH含量明显降低,差异均有统计学意义(P<0.01)。G-Rg1可以降低L-02细胞ROS及8-OHdG水平,提高线粒体膜电位,减轻了氟化钠所导致的DNA损伤,降低了MDA水平,提高了GSH水平,差异均有统计学意义(P<0.05,P<0.01)。结论:一定剂量范围的G-Rg1对氟化钠所导致的L-02细胞氧化应激损伤具有保护作用。

Objective ： To investigate the protective effects of Ginsenoside Rgl （ G - Rgl ） against oxidative damage induced by sodium fluoride（NaF） in L02 hepatocytes. Method：The L02 cells were cultured in vitro and were exposed to NaF for 24 h. The inhibitory effects of G- Rgl （20 ng/mL,40 ng/mL,80 ng/mL）were investigated simultaneously. Intracellular ROS generation and mitochondrial transmembrane potential were detected by flow cytometry analysis. The concentration of 8 - OHdG was detected by EL1SA. SCGE was used to detect the DNA damage of hepatocytes and the levels of MDA and GSH were detected. Results ： Compared with the control group, NaF obviously increased the relative levels of ROS and 8 - OHdG. The percentages of depolarized cells in hepatocytes exposed to NaF were significantly increased. The indices of DNA damaged cells, tail DNA, tail length and Olive tail moment were all s!gnificantly increased in NaF group. The con- centrations of MDA were increased, while the concentrations of GSH decreased. Treatment with G - Rgl inhibited the NaF - induced oxidative stress by reducing ROS production and 8 - OHdG levels, and mitochondrial depolarization. G - Rgl also decreased the indices of DNA damaged cells, tail DNA, tail length and Olive tail moment. Furthermore, G - Rg1 down - regulated the relative levels of MDA and up - regulated the levels of GSH. Conclusion ： G - Rgl might protect L02 ceils against oxidative damage induced by NaF.