下坡跑步通过AMPK通路诱导大鼠比目鱼肌线粒体自噬。

IF 3.7 3区 生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY
Huayu Shang, Ranggui Ma, Shengju Chen, Hao Deng, Mengyu Li, Shiqiao Zheng, He Zhang, Duo Zhang, Tianai Yang, Ying Yang, Zhi Xia
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引用次数: 0

摘要

众所周知,与同心运动相比,偏心运动更容易引起与迟发性肌肉酸痛相关的明显肌肉损伤。本研究旨在探讨amp激活的蛋白激酶(AMPK)通路是否参与控制大鼠骨骼肌对下坡跑步的线粒体自噬。88只雄性Sprague-Dawley大鼠在16°倾角16 m·min- 1的跑步机上运动90 min,于运动后0 h、12 h、24 h、48 h和72 h取样比目肌。运动前20分钟腹腔注射AMPK抑制剂化合物C或AMPK激活剂AICAR或生理盐水。下坡跑步后,骨骼肌线粒体结构出现异常,含有丝裂体;AMPK磷酸化、亲环蛋白D (CypD)、细胞色素C (CytC)、线粒体fk506结合蛋白8 (FKBP8)、微管相关蛋白1轻链3 (LC3)、FKBP8与LC3、线粒体动力蛋白相关蛋白1 (Drp1)、溶酶体相关膜蛋白2 (LAMP2)共定位表达水平显著升高;雷帕霉素磷酸化机制靶蛋白(mTOR Ser2448)和热休克蛋白60 (HSP60)、线粒体呼吸复合体I (NDUFB8)和复合体III (UQCRC2)的表达水平和三磷酸腺苷(ATP)含量均显著低于C组。进一步研究表明,复方C部分阻断了下坡跑步机跑步的效果,而AICAR则增强了这种效果。一组下坡跑步激活AMPK通路,促进LC3与线粒体和FKBP8共定位,诱导大鼠骨骼肌线粒体自噬和线粒体损伤。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Downhill running induced mitophagy in rat soleus muscle via the AMPK pathway.

Eccentric exercise is known to induce more pronounced muscle damage associated with delayed-onset muscle soreness than concentric exercise. This study aimed to investigate whether AMP-activated protein kinase (AMPK) pathway participates in control of mitophagy in rat skeletal muscle in response to downhill running. Eighty-eight male Sprague-Dawley rats were exercised on a treadmill tilted at 16° decline at 16 m·min- 1 for 90 min, with the soleus muscle sampled at 0 h, 12 h, 24 h, 48 h and 72 h after exercise. The AMPK inhibitor compound C or AMPK activator AICAR or saline was injected intraperitoneally 20 min before exercise. After downhill treadmill running, the skeletal muscle mitochondrial structure appeared to be abnormal and contained mitophagosomes; the expression levels of AMPK phosphorylation, cyclophilin D (CypD), cytochrome C (CytC), mitochondrial FK506-binding protein 8 (FKBP8), microtubule-associated protein 1 light chain 3 (LC3), and the co-localization of FKBP8 with LC3 and mitochondria with dynamin-related protein 1 (Drp1), lysosomal-associated membrane protein 2 (LAMP2) were significantly higher; the expression levels of mechanistic target of rapamycin (mTOR Ser2448) phosphorylation and heat shock protein 60 (HSP60), mitochondrial respiratory complex I (NDUFB8) and complex III (UQCRC2), and adenosine triphosphate (ATP) content were significantly lower than those in the C group. Further study showed that the effect of downhill treadmill running was partly blocked by compound C and strengthened by AICAR. A session of downhill treadmill running activated the AMPK pathway and promoted LC3 co-localizations with mitochondria and FKBP8, and induced mitophagy and mitochondrial damage within rat skeletal muscle.

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来源期刊
Journal of physiology and biochemistry
Journal of physiology and biochemistry 生物-生化与分子生物学
CiteScore
6.60
自引率
0.00%
发文量
86
审稿时长
6-12 weeks
期刊介绍: The Journal of Physiology and Biochemistry publishes original research articles and reviews describing relevant new observations on molecular, biochemical and cellular mechanisms involved in human physiology. All areas of the physiology are covered. Special emphasis is placed on the integration of those levels in the whole-organism. The Journal of Physiology and Biochemistry also welcomes articles on molecular nutrition and metabolism studies, and works related to the genomic or proteomic bases of the physiological functions. Descriptive manuscripts about physiological/biochemical processes or clinical manuscripts will not be considered. The journal will not accept manuscripts testing effects of animal or plant extracts.
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