Regular aerobic exercise-ameliorated troponin I carbonylation to mitigate aged rat soleus muscle functional recession
Regular aerobic exercise-ameliorated troponin I carbonylation to mitigate aged rat soleus muscle functional recession
复制标题
规律有氧运动改善肌钙蛋白I羰基化减轻老年大鼠比目鱼肌功能衰退
DOI：
10.1113/ep087564
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发表时间：
2019-05-01
影响因子：
2.7
通讯作者：
Yin, Dazhong
中科院分区：
文献类型：
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作者：
Liu, Wenfeng;Kuang, Heyu;Yin, Dazhong
本研究调查了羰基化在肌肉年龄相关功能衰退中的生物学作用，以及定期有氧运动如何影响不同于习惯性久坐行为的羰基化过程。24只健康雄性SD大鼠（平均年龄23月龄）随机分为老年安静对照组（O-SED）和老年有氧运动组（O-EX）。O-EX组参加常规有氧运动-跑步机跑步-运动强度在10周内从最大耗氧量（V-O2（max））的50-55%逐渐增加到65-70%。监测大鼠体重、运动行为指数、形态学和氧化应激。亲和素磁珠和电喷雾四极杆飞行时间质谱用于收集和分离羰基化蛋白，而蛋白质印迹检测分子靶点。O-SED和O-EX大鼠均具有19个蛋白质羰基化的氧化修饰位点。在O-SED组中，鉴定了16种特定的羰基化蛋白质，而在O-EX组中还发现了16种额外的特定物质，所有28种物质都表现出氧化修饰。羰基化的蛋白质包括肌钙蛋白I（TNNI 1;慢骨骼肌）、原肌球蛋白1和-辅肌动蛋白1。特别是，TNNI 1羰基化修饰仅在久坐大鼠中发现。有氧运动显著增加TNNI 1和Ca 2 +/钙调素依赖性蛋白激酶II的表达。观察结果表明，TNNI 1羰基化的定量可能是肌肉年龄相关功能衰退的潜在生物标志物。重要的是，规律的有氧运动似乎在肌肉中具有抗氧化作用，减少TNNI 1缓慢羰基化，促进Ca 2 +/钙调蛋白依赖性蛋白激酶II（CAMK 2）和TNNI 1表达，用于骨骼肌收缩调节，从而减轻可能与年龄相关的骨骼肌功能下降。
This study investigated the biological role of carbonylation in muscle age-related functional decline and how regular aerobic exercise may affect the carbonylation process differently from habitual sedentary behaviour. Twenty-four healthy male Sprague-Dawley (SD) rats (mean age: 23 months) were randomly divided into an old-aged sedentary control group (O-SED) and an old-aged aerobic exercise group (O-EX). The O-EX group participated in regular aerobic exercise - treadmill running - with exercise intensity increased gradually from 50-55% to 65-70% of maximum oxygen consumption (V-O2 (max)) over 10weeks. Rats' body weight, exercise behaviour index, morphology and oxidative stress were monitored. Avidin magnetic beads and electrospray ionization quadrupole time-of-flight mass spectrometry were used for gathering and separating carbonylated proteins while western blot tested for molecular targets. O-SED and O-EX rats both had 19 oxidative modification sites for protein carbonylation. In the O-SED group, 16 specific carbonylated proteins were identified, while 16 additional specific species were also found in the O-EX group, with all 28 species demonstrating oxidative modifications. The carbonylated proteins included troponin I (TNNI1; slow skeletal muscle), tropomyosin 1 and -actinin 1. In particular, TNNI1 carbonylation modifications were found only in sedentary rats. Aerobic exercise increased TNNI1 and Ca2+/calmodulin-dependent protein kinase II expression significantly. Observations suggested that quantification of TNNI1 carbonylation may be a potential biomarker of muscle age-related functional decline. Importantly, regular aerobic exercise appeared to have antioxidant effects in the muscle that reduced TNNI1 slow carbonylation and promoted Ca2+/calmodulin-dependent protein kinase II (CAMK2) and TNNI1 expression for skeletal muscle contraction regulation, thus attenuating possible age-related skeletal muscle functional decline.