Abstract：
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: 0 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 II 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 T-SOD 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.
摘要：
目的探讨二氢杨梅素(DHM)对小鼠运动性肌肉损伤(EIMD)的保护作用及其机制。方法将成年雄性C57BL/6J小鼠随机分为对照组,运动组（EG），运动+100mg/kg体重·dDHM（DHM）组。干预持续了四周,在此期间，EG和DHM组的动物每天进行1小时的运动训练。训练后的第二天,在EG和DHM组中进行了90分钟的跑步机运动（斜率：0和速度：18m/min）。运动后24小时，从三组中收集血液和腓肠肌样本，然后测定血清肌酸激酶(CK)和乳酸脱氢酶(LDH)活性,总超氧化物歧化酶(T-SOD)活性,丙二醛（MDA），和骨骼肌线粒体酶复合物I和II的活性。通过透射电子显微镜观察骨骼肌的组织学变化，免疫印迹法检测线粒体功能相关通路的蛋白表达。结果与EG组相比，DHM组骨骼肌形态改变和线粒体损伤减轻。DHM干预后，EIMD标记物CK和LDH的活性以及脂质过氧化水平受到显着抑制，血清T-SOD活性增强。Western印迹表明，沉默酶3型(SIRT3)的表达，雌激素相关受体α，DHM干预后，小鼠骨骼肌中过氧化物酶体增殖物激活受体-γ共激活因子-1α增加。结论DHM能减轻小鼠EIMD,可能通过SIRT3信号通路的激活促进高强度运动后小鼠骨骼肌线粒体结构和功能的恢复。
