PMID- 24676712
OWN - NLM
STAT- MEDLINE
DCOM- 20150105
LR  - 20140423
IS  - 1791-3004 (Electronic)
IS  - 1791-2997 (Linking)
VI  - 9
IP  - 6
DP  - 2014 Jun
TI  - Opposite effects of the gap junction blocker octanol on focal cerebral ischemia 
      occluded for different durations.
PG  - 2485-90
LID - 10.3892/mmr.2014.2075 [doi]
AB  - Protectants and executioners have been demonstrated to be used by gap junctions 
      in focal cerebral ischemia. Certain researchers hypothesized that the opposite 
      role of gap junctions may be associated with the injury extent, which has been 
      demonstrated to be highly correlated with occlusion duration. In order to examine 
      this hypothesis directly, the effects of octanol, a frequently used drug, were 
      examined to investigate the role of gap junctions, in rats following middle 
      cerebral artery occlusion (MCAO) for 30 min/2 h and 24 h reperfusion, 
      respectively. Octanol significantly reduced the infarct volume following 2 h of 
      occlusion concomitant with lower neurological deficits, whereas it enlarged the 
      infarct volume following 30 min of occlusion. Consistently, octanol attenuated 
      the number of transferase dUTP nick-end labeling (TUNEL) positive neurons in the 
      hippocampal CA1 region following 2 h of occlusion, while opposite effects were 
      observed for 30 min of occlusion. Further immunohistochemical studies 
      demonstrated that the expression of B-cell leukemia-2 (Bcl-2, anti-apoptotic 
      protein) was upregulated and that Bcl-2-associated X (Bax, proapoptotic protein) 
      was downregulated following 2 h of occlusion in the octanol group compared with 
      the ischemic group. Conversely, octanol downregulated the expression of the Bcl-2 
      protein concomitant with increased Bax protein following 30 min of occlusion. 
      These results indicated that the gap junction blocker octanol can protect against 
      ischemic injury following long-term occlusion, however, can aggravate ischemic 
      injury following short-term occlusion.
FAU - Ding, Wenting
AU  - Ding W
AD  - Department of Physiology, College of Fundamental Medical Science, Guangzhou 
      University of Chinese Medicine, Guangzhou, Guangdong 510006, P.R. China.
FAU - Zhou, Lequan
AU  - Zhou L
AD  - Department of Physiology, College of Fundamental Medical Science, Guangzhou 
      University of Chinese Medicine, Guangzhou, Guangdong 510006, P.R. China.
FAU - Liu, Wei
AU  - Liu W
AD  - Department of Physiology, College of Fundamental Medical Science, Guangzhou 
      University of Chinese Medicine, Guangzhou, Guangdong 510006, P.R. China.
FAU - Guan, Li
AU  - Guan L
AD  - Department of Physiology, College of Fundamental Medical Science, Guangzhou 
      University of Chinese Medicine, Guangzhou, Guangdong 510006, P.R. China.
FAU - Li, Xiaoying
AU  - Li X
AD  - Department of Physiology, College of Fundamental Medical Science, Guangzhou 
      University of Chinese Medicine, Guangzhou, Guangdong 510006, P.R. China.
FAU - Liu, Haimei
AU  - Liu H
AD  - Department of Physiology, College of Fundamental Medical Science, Guangzhou 
      University of Chinese Medicine, Guangzhou, Guangdong 510006, P.R. China.
FAU - Yan, Fuman
AU  - Yan F
AD  - Department of Physiology, College of Fundamental Medical Science, Guangzhou 
      University of Chinese Medicine, Guangzhou, Guangdong 510006, P.R. China.
FAU - Xu, Jinwen
AU  - Xu J
AD  - Department of Physiology, College of Fundamental Medical Science, Guangzhou 
      University of Chinese Medicine, Guangzhou, Guangdong 510006, P.R. China.
FAU - Zeng, Weiyong
AU  - Zeng W
AD  - Department of Physiology, College of Fundamental Medical Science, Guangzhou 
      University of Chinese Medicine, Guangzhou, Guangdong 510006, P.R. China.
FAU - Qiu, Min
AU  - Qiu M
AD  - Department of Physiology, College of Fundamental Medical Science, Guangzhou 
      University of Chinese Medicine, Guangzhou, Guangdong 510006, P.R. China.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20140327
PL  - Greece
TA  - Mol Med Rep
JT  - Molecular medicine reports
JID - 101475259
RN  - 0 (Octanols)
RN  - 0 (Proto-Oncogene Proteins c-bcl-2)
RN  - 0 (bcl-2-Associated X Protein)
SB  - IM
MH  - Animals
MH  - Brain Ischemia/*metabolism/pathology/physiopathology
MH  - Cerebral Infarction/metabolism/pathology/physiopathology
MH  - Gap Junctions/*drug effects
MH  - Gene Expression
MH  - Male
MH  - Octanols/administration & dosage/*pharmacology
MH  - Proto-Oncogene Proteins c-bcl-2/genetics/metabolism
MH  - Pyramidal Cells/metabolism
MH  - Rats
MH  - Time Factors
MH  - bcl-2-Associated X Protein/genetics/metabolism
EDAT- 2014/03/29 06:00
MHDA- 2015/01/06 06:00
CRDT- 2014/03/29 06:00
PHST- 2013/07/11 00:00 [received]
PHST- 2014/03/07 00:00 [accepted]
PHST- 2014/03/29 06:00 [entrez]
PHST- 2014/03/29 06:00 [pubmed]
PHST- 2015/01/06 06:00 [medline]
AID - 10.3892/mmr.2014.2075 [doi]
PST - ppublish
SO  - Mol Med Rep. 2014 Jun;9(6):2485-90. doi: 10.3892/mmr.2014.2075. Epub 2014 Mar 27.