红景天苷对自然衰老小鼠模型的抗衰老作用研究

目的通过检测红景天苷对自然衰老小鼠模型不同器官组织抗氧化酶活性及过氧化脂质水平的影响,探索红景天苷在老龄动物体内可能的抗衰老作用机制。方法使用不同剂量(0.2g/kg和1.0g/kg)的红景天苷给16月龄自然衰老小鼠灌胃60d后,检测小鼠血清、心脏、肝脏、肾脏和大脑等各器官组织匀浆中超氧化物歧化酶、谷胱甘肽过氧化酶的活性及过氧化脂质和脂褐素的水平。以人参皂苷为阳性药物。结果与未加药对照组相比,红景天苷高剂量给药组自然衰老小鼠的血清、心脏、肝脏及肾脏的超氧化物歧化酶活性显著提高,而血清、肝脏、肾脏中过氧化脂质水平显著下降。该高剂量给药组自然衰老小鼠的心脏、肝脏、肾脏和大脑中脂褐素水平均较对照组降低,其中尤以大脑中的脂褐素水平降低最为显著。此外,高剂量红景天苷给药组小鼠的肾脏和大脑中谷胱甘肽过氧化酶活性与对照组相比出现一定程度的升高。结论红景天苷能够有效提高自然衰老小鼠体内不同器官组织的抗氧化酶活性并且降低过氧化脂质和脂褐素水平,从而起到延缓衰老的作用。不同脏器组织对药物的反应性存在一定差异。

Research on the anti-aging role of salidroside in naturally aged mice

Objective To explore the possible anti-aging role of salidroside in naturally aged mice through testing the activity of antioxidant enzymes and the level of lipid peroxidation in some organs of the mice model. Methods Different doses ofsalidroside （0.2 g/kg and 1.0 g/kg） were administrated to the naturally aged mice （16-month-old） for 60 days. The activity of superoxide dismutase （SOD） and GSH-Peroxidase （GSH-Px）, as well as the level of Lipid peroxidation （LPO） and Lipofascin in multiple organs including plasma, heart, liver, kidney and brain of the mice was then detected and compared. Ginsenoside was used as a positive control. Results SOD activity was significantly increased in the plasma, heart, liver and kidney of the mice group treated with high-dose salidroside, while the level of LPO was decreased in the plasma, liver and kidney of the same group, as compared with untreated control. The level of lipofascin was decreased in the heart, liver, kidney and brain of the high-dose mice group, with the level of change in brain being more significant as compared with untreated control. Moreover, GSH-Px activity was increased in the kidney and brain of the mice treated with high-dose salidroside, when compared with untreated control group. Conclusion Salidroside plays an anti-aging role in vivo by increasing the activity of antioxidant enzymes and decreasing the level of lipid peroxidation in the naturally aged mice. The drug response may vary in different organs of the mice model.