人参皂甙Rg1与1,6-二磷酸果糖配伍抗疲劳作用的研究

To observe the compatible effect of ginsenoside Rg1 and 1, 6-fructose diphosphate on anti-fatigue, and to determine the optimal dose for compatibility, Male Kunming mice were randomized according to their body weight into 7 groups in total. 3 control groups (namely the quiet, exercise, and ginsenoside Rg1 control groups) and 4 treatment ones with different dosage of ginsenoside Rg1 and 1, 6-fructose diphosphate (namely Group A, Group B, Group C and Group D). The effect and interaction of ginsenoside Rg1 and 1, 6-fructose diphosphate on enhancing exercise tolerance were analyzed via factorial experiment design. Factorial analysis suggested significant difference in the duration of give-out swimming of mice between different dosage of ginsenoside Rg1 groups (P＜0.05). The duration of give-out swimming in all treatment groups witnessed significant extension, and the greatest extension was seen in group C. Compared to ginsenoside Rg1 control group, however, the duration in all treatment groups significantly lowered (P＜0.01). MDA content of group A was significantly lower than that of Group D and the exercise control group. The MDA content of all groups elevated compared to the quiet control group. The ratio between SOD and MDA in group A and C was significantly higher than the exercise control group, while the ratio in group C was significantly higher than the ginsenoside Rg1 control group. All groups witnessed a decline in SOD: MDA ratio compared to the quiet control group, and group D enjoyed the greatest significance (P＜0.01). LDH in group C and D was significantly lower than in the exercise and ginsenoside Rg1 control group (P＜0.05). As a result, compared to the exercise and ginsenoside Rg1 control group, compatibility reduced, to some extent, the impairment of myocardial and skeletal muscle cells, mitochondrion, and other ultrastructure of cells. Compatibility with 1, 6-fructose diphosphate did not extend the duration of give-out swimming of mice, however, it could reduce the impairment of myocardial and skeletal muscle cells, protect the respiratory function of mitochondrion to some extent, thus attenuate hypoxic cell damage.