鹰嘴豆源性鹰嘴豆芽素A对运动性疲劳大鼠的能量代谢调控作用

Regulatory Effect of Biochanin A on Energy Metabolism in Rats with Exercise-induced Fatigue

本研究探讨了鹰嘴豆芽素A(Biochanin A,Bio-A)的抗运动性疲劳(EIF)作用和能量代谢调控作用。本研究通过负重力竭游泳运动诱导了EIF大鼠模型。运动过程中对大鼠灌胃3个剂量(10,20和40 mg·kg^(-1)·d^(-1))的鹰嘴豆芽素A,同时腹腔注射0.5 mg·kg^(-1)·d^(-1)Compound C(AMPK抑制剂)。共运动或给药4周。分别检测大鼠的力竭时间、血清有害代谢物指标、能量代谢指标和骨骼肌氧化应激指标水平。通过RT-qPCR检测骨骼肌能量代谢基因转录水平。通过Western blot检测骨骼肌AMPKα的磷酸化水平。结果显示,鹰嘴豆芽素A剂量依赖性地升高了EIF大鼠的力竭时间,降低了LDH、CK和cTnI水平,升高了肝糖原、肌糖原和Glu水平,降低了LA和BUN水平,升高了SOD和CAT水平,降低了MDA水平,升高了PGC-1α、HK2、GLUT-4、CS的mRNA相对表达量,降低了PDK4的m RNA相对表达量,升高了AMPKα的相对磷酸化水平(P<0.05)。Compound C减弱了鹰嘴豆芽素A的抗疲劳作用(P<0.05)。总之,鹰嘴豆芽素A通过激活AMPK通路改善运动性疲劳大鼠的能量代谢,发挥抗疲劳作用,这一发现可能有助于进一步研究鹰嘴豆芽素A作为一种潜在的天然药物来预防和减轻运动性疲劳。

The purpose of this study was to explore the anti-exercise-induced fatigue(EIF)and energy metabolism regulation of Biochanin A(Bio-A).In this study,the EIF rat model was induced by weight-bearing exhaustive swimming.During exercise,rats were given intragastric administration of three doses of Biochanin A(10,20 and 40 mg·kg^(-1)·d^(-1)),and intraperitoneal injection of 0.5 mg·kg^(-1)·d^(-1)Compound C(AMPK inhibitor).Exercise or administration for 4 weeks.The exhaustion time,serum harmful metabolites,energy metabolism and oxidative stress of skeletal muscle were measured.The gene transcription level of energy metabolism in skeletal muscle was detected by RT-qPCR.The phosphorylation level of AMPKαin skeletal muscle was detected by Western blot.The results showed that Biochanin A increased the exhaustion time of EIF rats in a dose-dependent manner,decreased the levels of LDH,CK and cTnI,increased the levels of liver glycogen,muscle glycogen and Glu,decreased the levels of LA and BUN,increased the levels of SOD and CAT,decreased the level of MDA,increased the mRNA relative expression of PGC-1α,HK2,GLUT-4 and CS,decreased the mRNA relative expression of PDK4 and increased the relative phosphorylation level of AMPKα(P<0.05).Compound C attenuated the anti-fatigue effect of Biochanin A(P<0.05).In a word,Biochanin A can improve the energy metabolism of exercise-induced fatigue rats by activating AMPK pathway and play an anti-fatigue effect.This finding may facilitate further investigation of chickresin A as a potential natural drug to prevent and alleviate exercise fatigue.