益母草活性生物碱益母草碱对大鼠运动性疲劳的缓解作用

Ameliorative Effects of Leonurine,the Active Alkaloid from Leonurus japonicus,on Exercise-Induced Fatigue in Rats

本研究探讨了益母草的活性生物碱—益母草碱对大鼠运动性疲劳的缓解作用以及其调节Nrf2/Keap1/ARE信号通路的机制。实验采用动物模型,研究了益母草碱对骨骼肌的保护作用,探讨了它在调节抗氧化酶活性和降低细胞氧化应激中的作用。研究结果表明,益母草碱显著延长了大鼠的力竭游泳时间,降低了血清中的LDH、CK和cTnI水平,并显著提高了骨骼肌中SOD、CAT和GSH-Px的活性,减轻了MDA水平。这些发现揭示了益母草碱在减缓运动性疲劳中的显著作用。进一步的研究发现,益母草碱通过激活Nrf2/Keap1/ARE信号通路,增强了Nrf2及其下游靶基因HO-1和NQO-1的表达,抑制了Keap1的表达,为骨骼肌提供了更强的抗氧化防护。当使用Nrf2抑制剂ML385时,这一益母草碱的效果受到抑制,验证了其通过Nrf2/Keap1/ARE信号通路发挥作用的机制。本研究的结果表明,益母草碱作为一种天然的活性生物碱,具有显著的抗运动性疲劳作用,通过调节Nrf2/Keap1/ARE信号通路来减轻骨骼肌的氧化损伤,揭示了其作为一种新型抗疲劳天然化合物的巨大潜力。

This study explored the alleviative effects of leonurine,an active alkaloid from Leonurus japonicus(Chinese motherwort),on exercise-induced fatigue(EIF)in rats and its mechanism in regulating the Nrf2/Keap1/ARE signaling pathway.Using animal models,the experiment investigated the protective role of leonurine on skeletal muscles and its functions in modulating antioxidative enzyme activity and reducing cellular oxidative stress.The results revealed that leonurine significantly extended the exhaustive swimming time of rats,reduced serum levels of LDH,CK and cTnI,and notably increased the activity of SOD,CAT and GSH-Px in skeletal muscles,thereby reducing MDA levels.These findings unveiled the significant role of leonurine in mitigating exercise-induced fatigue.Further research discovered that leonurine activates the Nrf2/Keap1/ARE signaling pathway,enhancing the expression of Nrf2 and its downstream target genes HO-1 and NQO-1,while suppressing the expression of Keap1,providing stronger antioxidative protection to skeletal muscles.When the Nrf2 inhibitor ML385 was used,the effect of leonurine was inhibited,verifying its mechanism of action through the Nrf2/Keap1/ARE signaling pathway.The outcomes of this research indicate that leonurine,as a natural active alkaloid,has significant anti-EIF effects and reveals its substantial potential as a novel natural compound for anti-fatigue through modulating the Nrf2/Keap1/ARE signaling pathway to alleviate oxidative damage in skeletal muscles.