PMID- 25082329
OWN - NLM
STAT- MEDLINE
DCOM- 20150708
LR  - 20151119
IS  - 1097-4547 (Electronic)
IS  - 0360-4012 (Linking)
VI  - 93
IP  - 1
DP  - 2015 Jan
TI  - Postconditioning mitigates cell death following oxygen and glucose deprivation in 
      PC12 cells and forebrain reperfusion injury in rats.
PG  - 140-8
LID - 10.1002/jnr.23460 [doi]
AB  - Postconditioning mitigates ischemia-induced cellular damage via a modified 
      reperfusion procedure. Mitochondrial permeability transition (MPT) is an 
      important pathophysiological change in reperfusion injury. This study explores 
      the role of MPT modulation underlying hypoxic postconditioning (HPoC) in PC12 
      cells and studies the neuroprotective effects of ischemic postconditioning (IPoC) 
      on rats. Oxygen-glucose deprivation (OGD) was performed for 10 hr on PC12 cells. 
      HPoC was induced by three cycles of 10-min reoxygenation/10-min rehypoxia after 
      OGD. The MPT inhibitor N-methyl-4-isoleucine cyclosporine (NIM811) and the MPT 
      inducer carboxyatractyloside (CATR) were administered to selective groups before 
      OGD. Cellular death was evaluated by flow cytometry and Western blot analysis. 
      JC-1 fluorescence signal was used to estimate the mitochondrial membrane 
      potential ( big up tri, openPsim ). Transient global cerebral ischemia (tGCI) was induced via the 
      two-vessel occlusion and hypotension method in male Sprague Dawley rats. IPoC was 
      induced by three cycles of 10-sec reperfusion/10-sec reocclusion after index 
      ischemia. HPoC and NIM811 administration attenuated cell death, cytochrome c 
      release, and caspase-3 activity and maintained  big up tri, openPsim of PC12 cells after OGD. The 
      addition of CATR negated the protection conferred by HPoC. IPoC reduced neuronal 
      degeneration and cytochrome c release and cleaved caspase-9 expression of 
      hippocampal CA1 neurons in rats after tGCI. HPoC protected PC12 cells against OGD 
      by modulating the MPT. IPoC attenuated degeneration of hippocampal neurons after 
      cerebral ischemia.
CI  - (c) 2014 Wiley Periodicals, Inc.
FAU - Lin, Han-Chen
AU  - Lin HC
AD  - Department of Anatomy and Cell Biology, Medical College, National Taiwan 
      University, Taipei, Taiwan.
FAU - Narasimhan, Purnima
AU  - Narasimhan P
FAU - Liu, Shin-Yun
AU  - Liu SY
FAU - Chan, Pak H
AU  - Chan PH
FAU - Lai, I-Rue
AU  - Lai IR
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20140731
PL  - United States
TA  - J Neurosci Res
JT  - Journal of neuroscience research
JID - 7600111
RN  - 0 (Fluoresceins)
RN  - 0 (Formazans)
RN  - 0 (Tetrazolium Salts)
RN  - 0 (fluoro jade)
RN  - 23305-68-2 (MTT formazan)
RN  - 9007-43-6 (Cytochromes c)
RN  - EC 3.4.22.- (Caspase 3)
RN  - IY9XDZ35W2 (Glucose)
RN  - S88TT14065 (Oxygen)
SB  - IM
MH  - Animals
MH  - Caspase 3/metabolism
MH  - Cell Death/drug effects
MH  - Cytochromes c/metabolism
MH  - Disease Models, Animal
MH  - Flow Cytometry
MH  - Fluoresceins
MH  - Formazans
MH  - Glucose/*metabolism
MH  - Hippocampus/pathology
MH  - *Ischemic Postconditioning
MH  - Male
MH  - Membrane Potential, Mitochondrial
MH  - Oxygen/*metabolism
MH  - PC12 Cells
MH  - Rats
MH  - Reperfusion Injury/*pathology
MH  - Tetrazolium Salts
OTO - NOTNLM
OT  - hippocampus
OT  - hypoxia
OT  - mitochondrial permeability transition
OT  - neuronal ischemia
OT  - oxygen-glucose deprivation
OT  - postconditioning
EDAT- 2014/08/02 06:00
MHDA- 2015/07/15 06:00
CRDT- 2014/08/02 06:00
PHST- 2014/03/11 00:00 [received]
PHST- 2014/06/10 00:00 [revised]
PHST- 2014/07/05 00:00 [accepted]
PHST- 2014/08/02 06:00 [entrez]
PHST- 2014/08/02 06:00 [pubmed]
PHST- 2015/07/15 06:00 [medline]
AID - 10.1002/jnr.23460 [doi]
PST - ppublish
SO  - J Neurosci Res. 2015 Jan;93(1):140-8. doi: 10.1002/jnr.23460. Epub 2014 Jul 31.