目的 探讨人参皂苷Rg1防治阿尔茨海默病的作用机制.方法 将8.5月龄快速老化小鼠(SAMP8)随机分为SAMP8对照组、SAMP8给Rg1 10 mg/kg组、SAMP8给Rg1 30 mg/kg组,每组10只.同月龄SAMR1 10只作为对照组.给药65 d后提取肝脏线粒体,测定线粒体呼吸功能、线粒体肿胀度和线粒体膜电位.线粒体于-20℃/20℃反复冻融3次破坏线粒体膜,测定线粒体内MDA含量、SOD活性和LDH含量.结果 与SAMR1相比,SAMP8肝脏线粒体呼吸功能显著降低,表现为线粒体3态呼吸显著降低,4态呼吸改变不明显,呼吸控制指数和磷氧比值显著降低;SAMP8小鼠线粒体膜肿胀度显著增高,线粒体膜电位显著降低.此外,SAMP8线粒体MDA含量显著增多、SOD活性显著升高、LDH显著增高.与SAMP8对照组相比,Rg1 10 和30 mg/kg均可显著改善这些线粒体结构和呼吸功能障碍,改善线粒体内生化功能的改变.结论 人参皂苷Rg1可改善快速老化小鼠线粒体结构和功能障碍.%Objective To observe the influence of Rg1 on the mitochondria of senescence accelerated mice (SAM) to explore its mechanism on Alzheimer's disease (AD). Methods The 8?-month-old SAM were divided into SAM-prone/8 (SAMP8) group, SAMP8 treated with Rg1 10 mg/kg group and 30 mg/kg group. The same old SAM-resistance/1 (SAMR1) act as control. After treatment for 65 d, the liver mitochondria was isolated. Mitochondrial respiratory activity, mitochondrial membrane potential and mitochondrial swelling degree were determined. Mitochondrial oxidative stress was determined by measuring the level of lipid peroxidation and the activity of anti-oxidation enzymes. Results Respiratory control index (RCI), ADP/O ratio, State 3 respiration, and OPR were significantly lower in SAMP8 than those in SAMR1. State 4 respiration was no significantly change in SAMP8 compared with that in SAMR1. At the same time, the loss of mitochondrial membrane potential and the increase of mitochondrial swelling degree were found in SAMP8 liver mitochondria. Additionally, the level of MDA content was increased, the activity of SOD was decreased, and the LDH activity was increased in SAMP8 mitochondria compared with that in SAMR1 mitochondria. Rg1 10 mg/kg and 30 mg/kg significantly improved oxidative phosphorylation process, mitochondrial membrane potential, mitochondria swelling degree, and biochemical functions. Conclusions Rg1 can improve mitochondrial structure and function in SAMP8.
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