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|本期目录/Table of Contents|

间歇有氧运动训练上调SIRT3改善衰老心肌线粒体功能

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2015年第6期
页码:
645-649
栏目:
基础研究
出版日期:
2015-07-15

文章信息/Info

Title:
Aerobic interval training improves cardiac mitochondrial antioxidative function in aged heart via SIRT3 correction
作者:
马 颖1; 4; 马 恒2; 3; 刘敏4; 张 乐4; 李 妍4
(1.陕西省第四人民医院心内科，陕西 西安 710043；
第四军医大学：2.基础医学院生理学教研室，3.基础医学院病理生理学教研室，4.西京医院心血管内科，陕西 西安710032）
Author(s):
MA Ying1; 4;  MA Heng2; 3;  LIU Min4;  ZHANG Le4;  LI Yan4
(1.Department of Cardiology, Fourth People’s Hospital of Shaanxi Province, Xi’an 710043, Shaanxi, China；
2.Department of Physiology, 3.Department of Pathophysiology, Fourth Military Medical University, Xi’an 710032, Shaanxi, China, 4.Department of Cardiology, Xijing Hospital, Fourth Military Medical University, Xi’an 710032, Shaanxi, China)
关键词:
衰老; 间歇有氧运动训练; SIRT3; 线粒体; 心肌
Keywords:
aging;  aerobic interval training;  SIRT3;  mitochondria;  cardiomyocyte
分类号:
R540. 47
DOI:
-
文献标识码:
A
摘要:
目的 探讨间歇有氧运动训练（AIT）对调节SIRT3介导的抗氧化酶系统改善老年小鼠心肌线粒体功能的影响。方法 采用C57小鼠（20月龄）20只，随机分为AIT组和非运动组，每组10只。以成年野生型C57小鼠非运动组(4月龄，10只)为对照组。建立间歇有氧运动训练12周小鼠模型，跑台训练由3部分构成：10 min热身运动，7 min间歇训练（4 min高强度和3 min低强度训练）及1 min冷却。每日训练1 h，每周训练5 d，训练时间为12周。应用蛋白免疫印迹法(Western blot)检测心肌线粒体抗氧化酶相关蛋白的表达。结果 AIT显著上调衰老心肌中线粒体去乙酰化酶sirtuin-3（SIRT3）表达水平，提高AMP依赖的蛋白激酶(AMPK)的磷酸化水平(P<0.05)；AIT可改善老年组小鼠心肌线粒体抗氧化酶(MnSOD、Catalase)的活性，有效减少衰老心肌脂质过氧化损伤(P<0.05)；AIT训练显著提高衰老心肌线粒体生物合成能力改善了线粒体的功能(均P<0.05)。结论 有氧间歇运动训练可有效地上调衰老小鼠心肌细胞SIRT3水平，有效提高衰老小鼠心肌线粒体功能，其机制可能与激活心肌SIRT3所介导的抗氧化酶系统有关。
Abstract:
AIM To investigate the effect of aerobic interval training (AIT) on the cardiac mitochondrial function in aged mice hearts by SIRT3 mediated antioxidant enzyme system. METHODS Aged C57 mice (20 months) and adult C57 (4 months) mice were included in this study. AIT protocol consisted of 10-min warm-up period, 7-min interval training (4 min high-intensity and 3 min low-intensity training) and 1 min cool down. Training was performed for 1 h/day and 5 days/week for 12 weeks. Protein immune blot method (Western blot) was used to detect myocardial mitochondrial antioxidant enzyme related protein expressions. RESULTS AIT significantly increased the myocardial mitochondrial deacetylase sirtuin-3 (SIRT3) level and improved AMP-dependent protein kinase (AMPK) phosphorylation level in the aged hearts (P<0.05). Subsequently, AIT improved the activity of myocardial mitochondrial antioxidant enzymes (MnSOD, catalase) in the aged hearts. AIT also reduced the myocardial lipid peroxidation damage and improved the myocardial mitochondrial biosynthesis ability in the aged hearts (P<0.05). CONCLUSION AIT effectively increases the cardiomyocyte SIRT3 level in aged mice and improves myocardial mitochondrial functions. The cardioprotective mechanism of AIT may be related to the activation of myocardial SIRT3 mediated by the antioxidant enzyme system.

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备注/Memo

备注/Memo:
收稿日期：2015-01-23.讯作者：李妍，副教授，主要从事冠心病基础与临床研究Email：liyanfmmu@hotmail.com 共同
通讯作者：马恒，副教授，主要从事心肌内源性保护机制研究 Email：hengma@fmmu.edu.cn
作者简介：马颖，硕士生 Email：lovelyfoal@sina.com
更新日期/Last Update: 2015-07-23