潞党参通过PI3K/AKT/GSK3β通路缓解运动性疲劳的作用机制研究

Mechanism of Codonopsis Radix on Alleviating Exercise Fatigue Through PI3K/AKT/GSK3β Pathway

目的:对潞党参缓解运动性疲劳的作用及机制进行初步研究。方法:将小鼠随机分为对照组、人参总皂苷(20 mg/kg)阳性对照组及潞党参低(4.25 g/kg)、中(8.5 g/kg)、高(17 g/kg)剂量组,采用转棒实验和负重游泳实验评价潞党参缓解运动性疲劳的作用;采用生化检测方法检测小鼠血清LA、BUN、肝糖原、肌糖原及肝脏中T-SOD、MDA水平;运用蛋白免疫印迹法检测小鼠肝脏和骨骼肌中p-PI3K、p-AKT、p-GSK3β、GS蛋白表达。结果:与对照组比较,潞党参中、高剂量组小鼠转棒停留时间和负重游泳时间均显著延长,血清中BUN含量显著降低,肝糖原、肌糖原含量显著升高,肝脏中MDA含量显著降低,T-SOD活性显著升高,肝脏及骨骼肌中p-AKT、p-PI3K、p-GSK3β、GS蛋白表达显著升高,潞党参高剂量组血清LA水平显著降低(P<0.05~P<0.001)。结论:潞党参可能通过减少代谢产物堆积、促进抗氧化和升高糖原合成等途径起到缓解运动疲劳的作用,该作用机制可能与激活小鼠肝脏和骨骼肌中PI3K/AKT/GSK3β信号通路及相关蛋白GS有关。

Objective: To study the effect and mechanism of Codonopsis Radix on relieving exercise fatigue.Methods: The mice were randomly divided into control group, total saponins of Panax ginseng(20 mg/kg) positive control group and Codonopsis Radix low(4.25 g/kg),medium(8.5 g/kg),high(17 g/kg) dose groups.The effects of Codonopsis Radix on relieving exercise fatigue were evaluated by rod turning test and weight-bearing swimming test.The levels of serum LA,BUN,liver glycogen, muscle glycogen and liver T-SOD and MDA were detected by biochemical method.The protein expression levels of p-PI3K,p-AKT,p-GSK3β and GS in liver and skeletal muscle of mice were detected by Western Blot.Results: Compared with control group, the turn rod retention time and swimming time with weight loading of mice in Codonopsis Radix medium and high dose groups were significantly longer, the content of BUN in serum of mice were significantly decreased, the contents of liver glycogen and muscle glycogen were significantly increased, the content of MDA in liver was significantly decreased, and the activity of T-SOD was significantly increased, the protein expressions of p-AKT,p-PI3K,p-GSK3β and GS in liver and skeletal muscle were significantly increased, the level of serum LA was significantly decreased in Codonopsis Radix high dose group(P<0.05 to P<0.001).Conclusion: Codonopsis Radix may alleviate exercise fatigue by reducing the accumulation of metabolites, promoting antioxidant activity and increasing glycogen synthesis, the mechanism may be related to the activation of PI3K/AKT/GSK3β signaling pathway and related protein GS in mice liver and skeletal muscle.