Aerobic interval training protects against myocardial infarction-induced oxidative injury by enhancing antioxidase system and mitochondrial biosynthesis

作者：Jiang Hong Ke; Miao Yi; Wang You Hua; Zhao Mei; Feng Zhi Hui; Yu Xiao Jiang; Liu Jian Kang; Zang Wei Jin^*

来源：CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, 2014, 41(3): 192-201.

DOI：10.1111/1440-1681.12211

• aerobic interval training
• anti-oxidase
• mitochondrial biogenesis
• myocardial infarction
• phosphatidylinositol 3-kinase
• Akt signalling
• sirtuin 3

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 (20mg/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.

• 出版日期2014-3
• 单位西安交通大学; 南阳理工学院