二氢杨梅素对运动性骨骼肌损伤的保护作用及机制研究

吴瑛; 王大伟; 李军; 许贤杰; 高志丹; 李鸿雁; 张勇; 刘鹏

doi:10.24920/004272

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二氢杨梅素对运动性骨骼肌损伤的保护作用及机制研究

中国医学科学杂志（英文） 2024年39卷第1期页码：46-53

论著 | Updated：2024-05-27

- 二氢杨梅素对运动性骨骼肌损伤的保护作用及机制研究
- Affiliations：
  
  1. 1The Sixth Medical Center, Chinese People’s Liberation Army (PLA) General Hospital, Beijing 100048, China
  2. 2PLA Air Force Medical Center, Beijing 100142, China
  3. 3Rocket Army General Hospital, Chinese PLA General Hospital, Beijing 100088, China
  4. 4The Fourth Medical Center, Chinese PLA General Hospital, Beijing 100048, China
- Author bio：
  
  * 张勇，zhy-545@163.com；
  刘鹏，717344426@qq.com。
- Funds：
- DOI：10.24920/004272
  中图分类号：
- 收稿日期：2023-06-13，
  
  录用日期：2023-12-27，
  
  网络出版日期：2024-03-01，
  
  纸质出版日期：2024-03-31
- Accepted：
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吴瑛, 王大伟, 李军, 等. 二氢杨梅素对运动性骨骼肌损伤的保护作用及机制研究[J]. 中国医学科学杂志（英文）, 2024,39(1):46-53.

Ying Wu, Da-Wei Wang, Jun Li, et al. Protective Effect of Dihydromyricetin Against Exercise-Induced Muscle Damage and Its Mechanism[J]. Chinese medical sciences journal, 2024, 39(1): 46-53.
吴瑛, 王大伟, 李军, 等. 二氢杨梅素对运动性骨骼肌损伤的保护作用及机制研究[J]. 中国医学科学杂志（英文）, 2024,39(1):46-53. DOI： 10.24920/004272.

Ying Wu, Da-Wei Wang, Jun Li, et al. Protective Effect of Dihydromyricetin Against Exercise-Induced Muscle Damage and Its Mechanism[J]. Chinese medical sciences journal, 2024, 39(1): 46-53. DOI： 10.24920/004272.

摘要

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。

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.

关键词

Keywords

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