人参皂苷Rg1对运动性疲劳大鼠骨骼肌结构及功能的影响

Effects of Ginsenoside Rg1 on Structure and Function of Rat Skeletal Muscle with Exercise-induced Fatigue

【目的】观察人参皂苷Rg1对运动性疲劳大鼠骨骼肌结构及功能的影响。【方法】选用SD大鼠,随机分为空白组、模型组和人参皂苷Rg1组(剂量为50 mg.kg-1.d-1),后2组采用中等强度的跑台运动复制运动性疲劳大鼠模型。在给药后运动造模,连续2周,检测各组大鼠骨骼肌丙二醛(MDA)含量、超氧化物歧化酶(SOD)活性,线粒体膜电位和游离钙离子含量,并观察各组大鼠骨骼肌超微结构。【结果】模型组大鼠骨骼肌SOD活性、线粒体膜电位、游离钙离子含量均降低,MDA含量升高,与空白组比较差异均有显著性意义(P<0.01),骨骼肌细胞及其线粒体、细胞核等结构受损,出现凋亡。人参皂苷Rg1组可使大鼠骨骼肌SOD活性、线粒体膜电位、游离钙离子含量升高,MDA含量降低,与模型组比较差异均有显著性意义(P<0.01),骨骼肌肌纤维、细胞线粒体和细胞核等超微结构的损伤程度均较模型组减轻。【结论】人参皂苷Rg1抗运动性疲劳的作用可能与其能抑制运动所致自由基增加和脂质过氧化诱发骨骼肌细胞损伤有关。

Objective To observe the effects of ginsenoside Rgl group on the structure and function of rat skeletal muscle with exercise-induced fatigue. Methods SD rats were randomized into blank control group, model group and ginsenoside Rgl group. The rats in the model group and ginsenoside Rgl group received medium-intensity treadmill running to induce exercise-induced fatigue. Ginsenoside Rgl group was given ginsenoside Rgl 50 mg·kg^-1 · d^-1 for 2 continuous weeks during the modeling. After treatment, malondialdehyde （MDA） content, superoxide dismustase （SOD） activity, mitoehondrial membrane potential and free calcium content in the rat skeletal muscle were measured. Meanwhile, uhrastructure of the skeletal muscle was observed under the electron microscope. Results In the model group, SOD activity, mitochondrial membrane potential, and free calcium content were decreased, MDA content was increased, and the difference was significant as compared with the blank control group （P 〈0. 01 ）. The skeletal muscle cell and its mitochondria and nucleus were damaged in the model group, indicating the occurrence of apoptosis. Ginsenoside Rgl increased SOD activity, mitochondrial membrane potential, and free calcium content, decreased MDA content （P 〈0. 01 compared with the model group）, and reduced the damage of the skeletal muscle and its mitochondria and nucleus in model rats. Conclusion The mechanism of ginsenoside Rgl in counteracting exercise-induced fatigue is probably related with the inhibition of the skeletal muscle structure injury induced by exercise-induced free radical increase and lipid peroxidation.