Abstract：
Fatigue is a serious disturbance to human health, especially in people who have a severe disease such as cancer, or have been infected with COVID-19. Our research objective is to evaluate the anti-fatigue effect and mechanism of icariin through a mouse experimental model. Mice were treated with icariin for 30 days and anti-fatigue effects were evaluated by the weight-bearing swimming test, serum urea nitrogen test, lactic acid accumulation and clearance test in blood and the amount of liver glycogen. The protein expression levels of adenosine monophosphate-activated protein kinase (AMPK) and peroxisome proliferator-activated receptor-gamma coactivator-1alpha (PGC1-α) in the skeletal muscle of mice in each group were measured by western blotting. Results showed that icariin prolonged the weight-bearing swimming time of animals, reduced the serum urea nitrogen level after exercise, decreased the blood lactic acid concentration after exercise and increased the liver glycogen content observably. Compared to that in the control group, icariin upregulated AMPK and PGC1-α expression in skeletal muscle. Icariin can improve fatigue resistance in mice and its mechanism may be through improving the AMPK/PGC-1α pathway in skeletal muscle to enhance energy synthesis, decreasing the accumulation of metabolites and slowing glycogen consumption and decomposition.
摘要：
疲劳是对人类健康的严重干扰,尤其是患有严重疾病如癌症的人，或者已经感染了COVID-19。我们的研究目的是通过小鼠实验模型评估淫羊藿苷的抗疲劳作用和机制。用淫羊藿苷治疗小鼠30天，并通过负重游泳试验评估抗疲劳效果，血清尿素氮测试，乳酸在血液中的积累和清除试验以及肝糖原的量。采用蛋白质印迹法检测各组小鼠骨骼肌中腺苷酸活化蛋白激酶(AMPK)和过氧化物酶体增殖物激活受体-γ共激活因子-1α(PGC1-α)的蛋白表达水平。结果表明，淫羊藿苷延长了动物的负重游泳时间，降低运动后血清尿素氮水平，运动后血乳酸浓度降低，肝糖原含量增加。与对照组相比，淫羊藿苷上调骨骼肌中AMPK和PGC1-α的表达。淫羊藿苷能提高小鼠的抗疲劳性,其机制可能是通过改善骨骼肌AMPK/PGC-1α通路,促进能量合成,减少代谢产物的积累，减缓糖原的消耗和分解。
