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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 effect of ginsenoside Rg1 (G-Rg1) on mitochondrial oxidative damage induced by sodium fluoride in L-02 cells. Methods: Liver L-02 cells were cultured in vitro and treated with 4mM sodium fluoride for 24 hours. G-Rg1 was administered at doses of 20 ng / mL, 40 ng / mL and 80 ng / mL, respectively. DCFH-DA fluorescent probe to detect intracellular ROS content; JC-1 fluorescent probe to detect changes in mitochondrial membrane potential; Elisa method to detect intracellular 8-OHdG content; single cell gel electrophoresis technology to detect DNA damage; simultaneous detection Cell MDA, GSH content changes. Results: Compared with the normal control group, the levels of ROS and 8-OHdG in the sodium fluoride-treated group were significantly increased, the mitochondrial membrane potential was decreased, the tailing rate, tail length and Olive tail moment were significantly increased, and MDA content was significantly increased , GSH content was significantly lower, the difference was statistically significant (P <0.01). G-Rg1 could reduce the levels of ROS and 8-OHdG in L-02 cells, increase the mitochondrial membrane potential, reduce the DNA damage induced by sodium fluoride, decrease the level of MDA and increase the level of GSH (P <0.05, P <0.01). CONCLUSION: G-Rg1 at a dose range has a protective effect on L-02 cell oxidative stress induced by sodium fluoride.