二氢杨梅素对运动性骨骼肌损伤的保护作用及机制研究

Protective Effect of Dihydromyricetin Against Exercise-Induced Muscle Damage and Its Mechanism

目的探讨二氢杨梅素(dihydromyricetin,DHM)对运动训练后小鼠骨骼肌损伤的保护作用及潜在机制。方法将成年雄性C57BL/6J小鼠随机分为安静对照组(CG)、运动组(EG)、二氢杨梅素(100mg/kg·d)+运动组(DHM组)。干预期4周,同时进行运动训练,每天1小时。训练结束后的次日,EG组和DHM组进行一次坡度为0、速度为18 m/min、持续90 min的跑台运动。运动结束后24小时按组别取材,测定血清肌酸激酶(creatine kinase,CK)、乳酸脱氢酶(lactate dehydrogenase,LDH)和总超氧化物歧化酶(total superoxide dismutase,T-SOD)活性、丙二醛(malondialdehyde,MDA)含量和骨骼肌线粒体酶复合体Ⅰ和Ⅱ的活性,观察骨骼肌病理学组织形态变化。免疫印迹法(Western blot)检测线粒体功能相关通路的蛋白表达。结果与EG组相比,DHM组小鼠骨骼肌形态改变和线粒体损伤明显减轻。DHM显著抑制了运动后骨骼肌损伤的标志物CK和LDH及脂质过氧化水平,提高了骨骼肌T-SOD活性。Western blot结果显示,DHM显著增加小鼠骨骼肌沉默调节蛋白3(SIRT3)、雌激素相关受体α(EERα)和过氧化物酶体增殖物激活受体-γ共激活因子-1α(peroxisome proliferator-activated receptor gamma coactivator-1 alpha,PGC-1α)的表达。结论DHM有助于减轻小鼠运动性骨骼肌损伤,其机制可能是DHM可激活肌肉SIRT3信号通路,促进大强度运动后骨骼肌线粒体结构和功能的恢复。

Objective To investigate the protective effect of dihydromyricetin(DHM)against exercise-induced muscle damage(EIMD)in mice and its potential mechanism.Methods Adult male C57BL/6J mice were randomly divided into control group(CG),exercise group(EG),and exercise+100 mg/kg weight-d DHM(DHM)group.The intervention lasted for four weeks,during which the animals in the EG and DHM groups were subjected to exercise training for 1 h per day.The day after the training,a 90-min treadmill exercise(slope:O and speed:18 m/min)was conducted in both EG and DHM groups.Samples of blood and gastrocnemius muscles were harvested from the three groups 24 h after the exercise,followed by the measurement of serum creatine kinase(CK)and lactate dehydrogenase(LDH)activities,total superoxide dismutase(T-SOD)activity,malondialdehyde(MDA),and skeletal muscle mitochondrial enzyme complex I and I activities.Histological changes in the skeletal muscle were observed by transmission electron microscopy,and the protein expressions of mitochondrial function-related pathways were detected by Western blotting.Results Skeletal muscle morphological changes and mitochondrial damage were alleviated in the DHM group compared to those in the EG.The activities of EIMD markers CK and LDH and the level of lipid peroxidation were notably repressed and the serum TSOD activity was enhanced after DHM intervention.Western blotting demonstrated that the expressions of sirtuin type 3(SIRT3),estrogen-related receptor alpha,and peroxisome proliferator-activated receptor-gamma coactivator-1 alpha in the skeletal muscle of mice increased after the DHM intervention.Conclusion DHM can relieve EIMD in mice,possibly by promoting the recovery of the mitochondrial structure and function in the skeletal muscle of mice after high-intensity exercise via the activation of the SIRT3 signaling pathway.