鱼腥草黄酮对运动疲劳大鼠骨骼肌能量代谢的影响

Effects of Houttuynia cordata flavonoids on energy metabolism of skeletal muscle in exercise-induced fatigue rats

中文关键词:  鱼腥草  黄酮  运动疲劳  骨骼肌  线粒体  能量代谢

英文关键词:Houttuynia cordata  flavone  exercise-induced fatigue  skeletal muscle  mitochondrion  energy metabolism

中文摘要:

      目的 探究鱼腥草黄酮(Houttuynia cordata flavonoids, HCF)的抗疲劳作用及对运动疲劳大鼠骨骼肌能量代谢的影响。方法 通过灌胃低、中、高剂量HCF, 测定大鼠疲劳相关生化指标和骨骼肌线粒体能量代谢酶活性及相关基因表达水平。结果 与运动对照组相比, 低、中、高剂量组大鼠游泳时间得到显著提高(P<0.05), 分别提高了19.21%、38.41%、58.27%, 肝糖原、肌糖原含量分别提高了21.01% (P<0.01)、42.79% (P<0.01)、57.58% (P<0.01)和4.85%、36.43% (P<0.01)、62.17% (P<0.01), 并显著降低了血乳酸、血尿素氮含量和肌酸激酶、乳酸脱氢酶活性(P<0.05或P<0.01); 另外, 显著提高了骨骼肌线粒体中三磷酸腺苷(adenosine triphosphate, ATP)含量以及Ca2+-ATP水解酶、H+-ATP酶活性(P<0.05或P<0.01), 显著降低了骨骼肌的氧化应激水平, 同时激活了腺苷酸活化蛋白激酶(AMP-activated protein kinase, AMPK)/过氧化物酶体增殖物激活受体-γ共激活因子-1α (peroxisome proliferator-activated receptor-1α, PGC-1α)信号通路, 提高了AMPK、PGC-1α、过氧化物酶体增殖物激活受体α (peroxisome proliferator-activated receptorα, PPARα)、葡萄糖转运蛋白(recombinant glucose transporter, GLUT)的mRNA的表达水平。结论 HCF可以显著提高大鼠的运动耐力, 且呈剂量依赖关系, 其作用机制可能与骨骼肌线粒体的能量代谢和AMPK/PGC-1α信号通路有关。

英文摘要:

      Objective To investigate the anti-fatigue effect of Houttuynia cordata flavonoids (HCF) and its effects on energy metabolism in skeletal muscle mitochondria in exercise-induced fatigue rats. Methods Low, middle and high doses of HCF were given to rats by gavage to determine the fatigue-related biochemical indexes, the activity of energy metabolism enzymes in skeletal muscle mitochondria and the expression levels of related genes. Results Compared with the exercise control group, the swimming time of the low, medium, and high dose groups of rats was significantly improved (P<0.05), with increases of 19.21%, 38.41%, and 58.27%, respectively. The content of liver glycogen and muscle glycogen were increased by 21.01% (P<0.01), 42.79% (P<0.01), 57.58% (P<0.01), and 4.85%, 36.43% (P<0.01), and 62.17% (P<0.01), respectively, and blood lactate, blood urea nitrogen content, creatine kinase, and lactate dehydrogenase activity were significantly reduced (P<0.05 or P<0.01); in addition, it also increased the content of ATP and the activities of Ca2+-ATPase and H+-ATPase in skeletal muscle mitochondria (P<0.05 or P<0.01), decreased the oxidative stress of skeletal muscle, and activated the amp-activated protein kinase (AMPK)/peroxisome proliferator-activated receptor-1α (PGC-1α) signaling pathway, the mRNA expression levels of AMPK, PGC-1α, peroxisome proliferator- activated receptor α (PPARα) and recombinant glucose transporter (GLUT) were increased. Conclusion HCF can significantly improve the exercise endurance of rats in a dose-dependent manner, and its mechanism may be related to the energy metabolism of skeletal muscle mitochondria and AMPK/PGC-1α signaling pathway.