PMID- 24337985
OWN - NLM
STAT- MEDLINE
DCOM- 20141214
LR  - 20211021
IS  - 1559-1166 (Electronic)
IS  - 0895-8696 (Linking)
VI  - 53
IP  - 1
DP  - 2014 May
TI  - Ischemic postconditioning protects the neurovascular unit after focal cerebral 
      ischemia/reperfusion injury.
PG  - 50-8
LID - 10.1007/s12031-013-0196-0 [doi]
AB  - Recently, cerebral ischemic postconditioning (Postcond) has been shown to reduce 
      infarction volume in cerebral ischemia/reperfusion (I/R) injury. However, it is 
      unclear if ischemic Postcond offers more extensive neuroprotection than current 
      therapies. The aim of this study was to investigate the neuroprotective effects 
      of ischemic Postcond on the neurovascular unit (NVU). A middle cerebral artery 
      occlusion rat model was used; cerebral infarct volumes, neurologic scores, and 
      transmission electron microscopy were evaluated 24 h after reperfusion. We used 
      Evans blue extravasation, immunohistochemistry, and Western blot analyses to 
      evaluate the integrity of the blood brain barrier (BBB) and the distribution and 
      expression of the tight junction (TJ)-associated proteins of claudin-5 and 
      occludin in brain microvessel endothelium. The Postcond group showed 
      significantly reduced infarct volumes and decreased neurologic impairment scores 
      compared to the I/R group. Also, injuries to the cerebral microvascular 
      endothelial cells, astrocytes, and neurons were minimized in the Postcond group. 
      The permeability of the BBB increased in both the I/R and Postcond groups, but 
      the Postcond group showed a significant decrease in permeability than the I/R 
      group. Expression of both claudin-5 and occludin were higher in the Postcond 
      groups compared to the I/R group, but expression of both proteins decreased in 
      the I/R and Postcond groups compared to the sham group. The results of our study 
      suggest that ischemic Postcond is an effective way to reduce injury to neurons, 
      astrocytes, and endothelial cells, to increase protein expressions of 
      TJ-associated proteins, and to improve BBB intergrity affected by focal I/R. 
      Ischemic Postcond could protect the NVU from I/R injury.
FAU - Han, Dong
AU  - Han D
AD  - Department of Neurology, The Affiliated Shengjing Hospital of China Medical 
      University, No. 36 Sanhao Street, Heping District, Shenyang, Liaoning, 110004, 
      China.
FAU - Zhang, Shuo
AU  - Zhang S
FAU - Fan, Bin
AU  - Fan B
FAU - Wen, Lu-Lu
AU  - Wen LL
FAU - Sun, Miao
AU  - Sun M
FAU - Zhang, Hong
AU  - Zhang H
FAU - Feng, Juan
AU  - Feng J
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20131212
PL  - United States
TA  - J Mol Neurosci
JT  - Journal of molecular neuroscience : MN
JID - 9002991
RN  - 0 (Tight Junction Proteins)
RN  - 45PG892GO1 (Evans Blue)
SB  - IM
MH  - Animals
MH  - Blood-Brain Barrier/metabolism/pathology
MH  - *Capillary Permeability
MH  - Cerebral Cortex/*blood supply/metabolism
MH  - Evans Blue/pharmacokinetics
MH  - Infarction, Middle Cerebral Artery/metabolism/*therapy
MH  - *Ischemic Postconditioning
MH  - Rats
MH  - Reperfusion Injury/metabolism/*therapy
MH  - Tight Junction Proteins/genetics/metabolism
EDAT- 2013/12/18 06:00
MHDA- 2014/12/17 06:00
CRDT- 2013/12/17 06:00
PHST- 2013/10/21 00:00 [received]
PHST- 2013/11/26 00:00 [accepted]
PHST- 2013/12/17 06:00 [entrez]
PHST- 2013/12/18 06:00 [pubmed]
PHST- 2014/12/17 06:00 [medline]
AID - 10.1007/s12031-013-0196-0 [doi]
PST - ppublish
SO  - J Mol Neurosci. 2014 May;53(1):50-8. doi: 10.1007/s12031-013-0196-0. Epub 2013 
      Dec 12.