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- Title
Aerobic interval training protects against myocardial infarction-induced oxidative injury by enhancing antioxidase system and mitochondrial biosynthesis.
- Authors
Jiang, Hong‐Ke; Miao, Yi; Wang, You‐Hua; Zhao, Mei; Feng, Zhi‐Hui; Yu, Xiao‐Jiang; Liu, Jian‐Kang; Zang, Wei‐Jin
- Abstract
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 ( SIRT3) and the prosurvival phosphatidylinositol-3 kinase ( PI3-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 SIRT3 levels and PI3-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 SIRT3 upregulation and PI3-K/Akt signalling activation. Moreover, PI3-K inhibitor- LY294002 (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 SIRT3 expression and activation of PI3-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.
- Subjects
INTERVAL training; CORONARY disease; MYOCARDIAL infarction; PROTEIN kinases; ENZYMES
- Publication
Clinical & Experimental Pharmacology & Physiology, 2014, Vol 41, Issue 3, p192
- ISSN
0305-1870
- Publication type
Article
- DOI
10.1111/1440-1681.12211