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Aerobic interval training protects against myocardial infarction‐induced oxidative injury by enhancing antioxidase system and mitochondrial biosynthesis
Author(s) -
Jiang HongKe,
Miao Yi,
Wang YouHua,
Zhao Mei,
Feng ZhiHui,
Yu XiaoJiang,
Liu JianKang,
Zang WeiJin
Publication year - 2014
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/1440-1681.12211
Subject(s) - mitochondrial biogenesis , ampk , protein kinase b , mitochondrion , oxidative phosphorylation , amp activated protein kinase , medicine , endocrinology , oxidative stress , protein kinase a , tfam , biology , chemistry , kinase , biochemistry , phosphorylation
Summary Aerobic interval training ( AIT ) exerts beneficial effects on cardiovascular disease. However, its cardioprotective mechanisms are not fully understood. The aim of the present study was to evaluate AIT ‐mediated anti‐oxidation by focusing on anti‐oxidase and mitochondrial biogenesis in rats after myocardial infarction ( MI ). Sprague–Dawley rats were divided into three groups: (i) a sham‐operated control ( CON ); (ii) an MI group; and (iii) an MI + AIT group. Myocardial microstructure and function, markers of oxidative stress, mitochondrial anti‐oxidase, Phase II enzymes and mitochondrial biogenesis were assessed. In addition, levels of nuclear factor‐erythroid 2‐related factor (Nrf2) and phosphorylated (p‐) AMP ‐activated protein kinase ( AMPK ) were determined. The anti‐oxidative gene sirtuin 3 ( SIRT 3 ) and the prosurvival phosphatidylinositol‐3 kinase ( PI 3‐K)‐protein kinase B (Akt) signalling cascade were also evaluated. Compared with CON , there was noticeable microstructure injury, cardiac dysfunction and oxidative damage in rats after MI . In addition, decreased mitochondrial anti‐oxidase content, Phase II enzyme (except heme oxygenase‐1) expression and mitochondrial biogenesis were observed in the post‐ MI rats as well as reduced protein levels of the regulators Nrf2 and p‐ AMPK and suppression of SIRT 3 levels and PI 3‐K/Akt signalling. These detrimental modifications were considerably ameliorated by AIT , as evidenced by increases in anti‐oxidase, mitochondrial biogenesis, Nrf2 and AMPK phosphorylation, as well as SIRT 3 upregulation and PI 3‐K/Akt signalling activation. Moreover, PI 3‐K inhibitor‐ LY 294002 (20 mg/kg) treatment partly attenuated AIT ‐elicited increases in Nrf2 levels and AMPK phosphorylation. Based on these results, we conclude that AIT effectively alleviates MI ‐induced oxidative injury, which may be closely correlated with activation of the anti‐oxidase system and mitochondrial biosynthesis. Increased SIRT 3 expression and activation of PI 3‐K/Akt signalling may play key roles in AIT ‐mediated anti‐oxidation. These results open up new avenues for exercise intervention therapies for MI patients.