Oxidative stress in skeletal muscle exercise and injury

骨骼肌运动和损伤中的氧化应激

• 批准号: 16K01736
• 负责人: Wolf Alexander
• 金额: $ 2.66万
• 依托单位: Nippon Medical School
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 2016
• 资助国家: 日本
• 起止时间: 2016-04-01 至 2022-03-31
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-16K01736/
• 关键词: redox; exercise; injury; imaging; roGFP; DAMPs; 運動; 酸化ストレス; 活性酸素; GFP; イメージング

Exercise is a powerful intervention to increase health span in humans and widely advocated to prevent the functional decline occurring in old age. Exercise builds muscle mass, which prevents frailty, increases mobility, as a consequence, quality of life. Oxidative stress has long been seen as a negative consequence of exercise, but recent results suggest that reducing oxidative stress can prevent the beneficial effects of exercise. Using transgenic mice expressing a ratiometric redox-sensitive fluorescent protein (roGFP1) in mitochondrial or cytosol, we recorded the cellular redox state in skeletal muscle of live animals using in vivo confocal imaging.Activation of intact muscle alone did not cause any changes in the redox state of cytosol or mitochondria of muscle, but in a serendipitous discovery, electrical stimulation did induce oxidative stress in muscle fibers surrounding a single injured muscle fiber. Muscle fiber injury is a common occurrence in exercise, and seen as negative consequence of strenuous muscle activation. Our results indicate that muscle fiber injury probably plays an important role in mediating the redox signaling necessary for the beneficial effects of exercise. We tentatively conclude that danger associated molecular patterns (DAMPs) released by injured muscle fibers cause, together with muscle activation, the observed redox transients in adjacent tissue muscle fibers. Our findings resolve many conflicting observations concerning the role of oxidative stress and muscle injury in the benefits of exercise.

运动是一种有效的干预措施，可以增加人类的健康寿命，并被广泛提倡以防止老年人的功能下降。运动建立肌肉质量，防止脆弱，增加流动性，因此，生活质量.长期以来，氧化应激一直被认为是运动的负面后果，但最近的研究结果表明，减少氧化应激可以防止运动的有益效果。使用在线粒体或胞质溶胶中表达比率氧化还原敏感荧光蛋白（roGFP 1）的转基因小鼠，我们使用体内共聚焦成像记录了活动物骨骼肌中细胞的氧化还原状态。单独激活完整肌肉不会引起肌肉胞质溶胶或线粒体氧化还原状态的任何变化，但在一个偶然的发现中，电刺激确实在单个受损肌纤维周围的肌纤维中诱导氧化应激。肌纤维损伤是运动中常见的现象，被视为剧烈肌肉激活的负面后果。我们的研究结果表明，肌纤维损伤可能在介导运动有益效果所需的氧化还原信号中起着重要作用。我们初步得出结论，危险相关的分子模式（DAMPs）受伤的肌肉纤维释放的原因，连同肌肉激活，观察到的氧化还原瞬变在邻近组织的肌肉纤维。我们的研究结果解决了许多关于氧化应激和肌肉损伤在运动益处中的作用的相互矛盾的观察结果。

项目成果

UVA and UVB-induced oxidative stress in live mouse skin - lack of XPA prolongs recovery from oxidative stress -

UVA 和 UVB 诱导活体​​小鼠皮肤氧化应激 - 缺乏 XPA 可延长氧化应激恢复时间 -

• 发表时间: 2017
• 作者: Yoko Funasaka;Alexander M. Wolf;Naomi Kamimura;Yoichi Yabuki;Fumino Oda;Shigeo Ohta;Hidehisa Saeki
• 通讯作者: Hidehisa Saeki

ブルーライト照射による皮膚への酸化ストレス誘導

蓝光照射诱导皮肤氧化应激

• 发表时间: 2016
• 作者: Yoko Funasaka;Alexander M. Wolf;Naomi Kamimura;Yoichi Yabuki;Fumino Oda;Shigeo Ohta;Hidehisa Saeki;中嶋 裕也,Wolf Alexander,太田成男
• 通讯作者: 中嶋 裕也,Wolf Alexander,太田成男

糖尿病モデルマウスのin vivo酸化ストレス解析

糖尿病模型小鼠体内氧化应激分析

• 发表时间: 2017
• 作者: 上村尚美;Alexander M Wolf;西槙貴代美;横田隆;井内勝哉;太田成男
• 通讯作者: 太田成男

Dysfunctional mitochondria is accumulated by high glucose and albumin in HK-2 cells

HK-2 细胞中高葡萄糖和白蛋白导致功能失调的线粒体积累

• 发表时间: 2018
• 作者: 井本明美;黒崎祥史;Wolf Alexander M.;西村由香里;古田玲子;片桐真人; 石井直仁
• 通讯作者: 石井直仁

表皮幹細胞酸化還元状態のIn vivo イメージング

表皮干细胞氧化还原状态的体内成像

• 发表时间: 2016
• 作者: Yoko Funasaka;Alexander M. Wolf;Naomi Kamimura;Yoichi Yabuki;Fumino Oda;Shigeo Ohta;Hidehisa Saeki;中嶋 裕也,Wolf Alexander,太田成男;Alexander Wolf,太田成男
• 通讯作者: Alexander Wolf,太田成男