PMID- 24471974
OWN - NLM
STAT- MEDLINE
DCOM- 20141110
LR  - 20171116
IS  - 1440-1681 (Electronic)
IS  - 0305-1870 (Linking)
VI  - 41
IP  - 3
DP  - 2014 Mar
TI  - Aerobic interval training protects against myocardial infarction-induced 
      oxidative injury by enhancing antioxidase system and mitochondrial biosynthesis.
PG  - 192-201
LID - 10.1111/1440-1681.12211 [doi]
AB  - 1. 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). 2. 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. 3. 
      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. 4. 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.
CI  - (c) 2014 Wiley Publishing Asia Pty Ltd.
FAU - Jiang, Hong-Ke
AU  - Jiang HK
AD  - Department of Pharmacology, College of Medicine, Xi'an Jiaotong University, 
      Xi'an, China; Department of Physical Education, Nan Yang Institute of Technology, 
      Nan Yang, China.
FAU - Miao, Yi
AU  - Miao Y
FAU - Wang, You-Hua
AU  - Wang YH
FAU - Zhao, Mei
AU  - Zhao M
FAU - Feng, Zhi-Hui
AU  - Feng ZH
FAU - Yu, Xiao-Jiang
AU  - Yu XJ
FAU - Liu, Jian-Kang
AU  - Liu JK
FAU - Zang, Wei-Jin
AU  - Zang WJ
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Australia
TA  - Clin Exp Pharmacol Physiol
JT  - Clinical and experimental pharmacology & physiology
JID - 0425076
RN  - 0 (Antioxidants)
RN  - 0 (NF-E2-Related Factor 2)
RN  - EC 2.7.1.137 (Phosphatidylinositol 3-Kinase)
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
RN  - EC 2.7.11.31 (AMP-Activated Protein Kinases)
RN  - EC 3.5.1.- (Sirtuin 3)
SB  - IM
MH  - AMP-Activated Protein Kinases/metabolism
MH  - Animals
MH  - Antioxidants/*metabolism
MH  - Male
MH  - Mitochondria/*metabolism/physiology
MH  - Mitochondrial Turnover/*physiology
MH  - Myocardial Infarction/metabolism/*physiopathology
MH  - NF-E2-Related Factor 2/metabolism
MH  - Oxidation-Reduction
MH  - Oxidative Stress/*physiology
MH  - Phosphatidylinositol 3-Kinase/metabolism
MH  - Physical Conditioning, Animal/*physiology
MH  - Proto-Oncogene Proteins c-akt/metabolism
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Sirtuin 3/metabolism
OTO - NOTNLM
OT  - aerobic interval training
OT  - anti-oxidase
OT  - mitochondrial biogenesis
OT  - myocardial infarction
OT  - phosphatidylinositol 3-kinase/Akt signalling
OT  - sirtuin 3
EDAT- 2014/01/30 06:00
MHDA- 2014/11/11 06:00
CRDT- 2014/01/30 06:00
PHST- 2013/08/01 00:00 [received]
PHST- 2014/01/02 00:00 [revised]
PHST- 2014/01/03 00:00 [accepted]
PHST- 2014/01/30 06:00 [entrez]
PHST- 2014/01/30 06:00 [pubmed]
PHST- 2014/11/11 06:00 [medline]
AID - 10.1111/1440-1681.12211 [doi]
PST - ppublish
SO  - Clin Exp Pharmacol Physiol. 2014 Mar;41(3):192-201. doi: 10.1111/1440-1681.12211.