PMID- 26769958
OWN - NLM
STAT- MEDLINE
DCOM- 20161227
LR  - 20171116
IS  - 1522-1601 (Electronic)
IS  - 0161-7567 (Linking)
VI  - 120
IP  - 8
DP  - 2016 Apr 15
TI  - Effect of superoxide anion scavenger on rat hearts with chronic intermittent 
      hypoxia.
PG  - 982-90
LID - 10.1152/japplphysiol.01109.2014 [doi]
AB  - Only very limited information regarding the protective effects of the superoxide 
      anion scavenger on chronic intermittent hypoxia-induced cardiac apoptosis is 
      available. The purpose of this study is to evaluate the effects of the superoxide 
      anion scavenger on cardiac apoptotic and prosurvival pathways in rats with sleep 
      apnea. Forty-two Sprague-Dawley rats were divided into three groups, rats with 
      normoxic exposure (Control, 21% O2, 1 mo), rats with chronic intermittent hypoxia 
      exposure (Hypoxia, 3-7% O2vs. 21% O2per 40 s cycle, 8 h per day, 1 mo), and rats 
      with pretreatment of the superoxide anion scavenger and chronic intermittent 
      hypoxia exposure (Hypoxia-O2 (-)-Scavenger, MnTMPyP pentachloride, 1 mg/kg ip per 
      day; 3-7% O2vs. 21% O2per 40 s cycle, 8 h per day, 1 mo) at 5-6 mo of age. After 
      1 mo, the protein levels and apoptotic cells of excised hearts from three groups 
      were measured by Western blotting and terminal deoxynucleotide 
      transferase-mediated dUTP nick end labeling (TUNEL) assay. The superoxide anion 
      scavenger decreased hypoxia-induced myocardial architecture abnormalities, left 
      ventricular hypertrophy, and TUNEL-positive apoptosis. The superoxide anion 
      scavenger decreased hypoxia-induced Fas ligand, Fas death receptors, 
      Fas-associated death domain (FADD), activated caspase-8, and activated caspase-3 
      (Fas-dependent apoptotic pathway) as well as Bad, activated caspase-9 and 
      activated caspase-3 (mitochondria-dependent apoptotic pathway), endonuclease G 
      (EndoG), apoptosis-inducing factor (AIF), and TUNEL-positive apoptosis. The 
      superoxide anion scavenger increased IGF-1, IGF-1R, p-PI3k, p-Akt, p-Bad, Bcl-2, 
      and Bcl-xL (survival pathway). Our findings imply that the superoxide anion 
      scavenger might prevent cardiac Fas-mediated and mitochondrial-mediated apoptosis 
      and enhance the IGF-1-related survival pathway in chronic intermittent hypoxia. 
      The superoxide anion scavenger may prevent chronic sleep apnea-enhanced cardiac 
      apoptotic pathways and enhances cardiac survival pathways.
CI  - Copyright (c) 2016 the American Physiological Society.
FAU - Pai, Peiying
AU  - Pai P
AD  - China Medical University, Graduate Institute of Clinical Medical Science, 
      Taichung, Taiwan; Division of Cardiology, Department of Internal Medicine, China 
      Medical University Hospital, Taichung, Taiwan;
FAU - Lai, Ching Jung
AU  - Lai CJ
AD  - Department of Physiology, Tzu Chi University, Hualien, Taiwan;
FAU - Lin, Ching-Yuang
AU  - Lin CY
AD  - China Medical University, Graduate Institute of Clinical Medical Science, 
      Taichung, Taiwan; Clinical Immunology Center, China Medical University Hospital, 
      Taichung, Taiwan;
FAU - Liou, Yi-Fan
AU  - Liou YF
AD  - Division of Cardiology, Department of Internal Medicine, China Medical University 
      Hospital, Taichung, Taiwan;
FAU - Huang, Chih-Yang
AU  - Huang CY
AD  - Graduate Institute of Chinese Medical Science, China Medical University, 
      Taichung, Taiwan; Institute of Basic Medical Science, China Medical University, 
      Taichung, Taiwan; Department of Health and Nutrition Biotechnology, Asia 
      University, Taichung, Taiwan;
FAU - Lee, Shin-Da
AU  - Lee SD
AD  - School of Rehabilitation Science, Shanghai University of Traditional Chinese 
      Medicine, Shanghai, China; Department of Occupational Therapy, Asia University, 
      Taichung, Taiwan; and Department of Physical Therapy, Graduate Institute of 
      Rehabilitation Science, China Medical University, Taichung, Taiwan 
      shinda@mail.cmu.edu.tw.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20160114
PL  - United States
TA  - J Appl Physiol (1985)
JT  - Journal of applied physiology (Bethesda, Md. : 1985)
JID - 8502536
RN  - 0 (Apoptosis Inducing Factor)
RN  - 0 (fas Receptor)
RN  - 11062-77-4 (Superoxides)
RN  - 67763-96-6 (Insulin-Like Growth Factor I)
RN  - EC 3.4.22.- (Caspases)
SB  - IM
MH  - Animals
MH  - Apoptosis/physiology
MH  - Apoptosis Inducing Factor/metabolism
MH  - Caspases/metabolism
MH  - Heart/*physiopathology
MH  - Hypoxia/metabolism/*physiopathology
MH  - Insulin-Like Growth Factor I/metabolism
MH  - Mitochondria, Heart/metabolism/physiology
MH  - Myocardium/metabolism
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Signal Transduction/physiology
MH  - Sleep Apnea Syndromes/metabolism/physiopathology
MH  - Superoxides/*metabolism
MH  - fas Receptor/metabolism
OTO - NOTNLM
OT  - Fas receptor
OT  - caspase
OT  - cell death
OT  - heart
OT  - hypoxia
OT  - survival
EDAT- 2016/01/16 06:00
MHDA- 2016/12/28 06:00
CRDT- 2016/01/16 06:00
PHST- 2014/12/15 00:00 [received]
PHST- 2016/01/08 00:00 [accepted]
PHST- 2016/01/16 06:00 [entrez]
PHST- 2016/01/16 06:00 [pubmed]
PHST- 2016/12/28 06:00 [medline]
AID - japplphysiol.01109.2014 [pii]
AID - 10.1152/japplphysiol.01109.2014 [doi]
PST - ppublish
SO  - J Appl Physiol (1985). 2016 Apr 15;120(8):982-90. doi: 
      10.1152/japplphysiol.01109.2014. Epub 2016 Jan 14.