PMID- 21960347
OWN - NLM
STAT- MEDLINE
DCOM- 20120202
LR  - 20211020
IS  - 1862-1783 (Electronic)
IS  - 1673-1581 (Print)
IS  - 1673-1581 (Linking)
VI  - 12
IP  - 10
DP  - 2011 Oct
TI  - Iptakalim, an ATP-sensitive potassium channel opener, confers neuroprotection 
      against cerebral ischemia/reperfusion injury in rats by protecting neurovascular 
      unit cells.
PG  - 835-45
LID - 10.1631/jzus.B1100067 [doi]
AB  - OBJECTIVE: To investigate the role of iptakalim, an ATP-sensitive potassium 
      channel opener, in transient cerebral ischemia/reperfusion (I/R) injury and its 
      involved mechanisms. METHODS: Intraluminal occlusion of middle cerebral artery 
      (MCAO) in a rat model was used to investigate the effect of iptakalim at 
      different time points. Infarct volume was measured by staining with 
      2,3,5-triphenyltetrazolium chloride, and immunohistochemistry was used to 
      evaluate the expressions of Bcl-2 and Bax. In vitro, neurovascular unit (NVU) 
      cells, including rat primary cortical neurons, astrocytes, and cerebral 
      microvascular endothelial cells, were cultured and underwent oxygen-glucose 
      deprivation (OGD). The protective effect of iptakalim on NVU cells was 
      investigated by cell viability and injury assessments, which were measured by 
      3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and release of 
      lactate dehydrogenase. Caspase-3, Bcl-2 and Bax mRNA expressions were evaluated 
      by real-time polymerase chain reaction (PCR). RESULTS: Administration of 
      iptakalim 0 or 1 h after reperfusion significantly reduced infarct volumes, 
      improved neurological scores, and attenuated brain edema after cerebral I/R 
      injury. Iptakalim treatment (0 h after reperfusion) also reduced caspase-3 
      expression and increased the ratio of Bcl-2 to Bax by immunohistochemistry. 
      Iptakalim inhibited OGD-induced cell death in cultured neurons and astrocytes, 
      and lactate dehydrogenase release from cerebral microvascular endothelial cells. 
      Iptakalim reduced mRNA expression of caspase-3 and increased the ratio of Bcl-2 
      to Bax in NVU cells. CONCLUSIONS: Iptakalim confers neuroprotection against 
      cerebral I/R injury by protecting NVU cells via inhibiting of apoptosis.
FAU - Ran, Yu-hua
AU  - Ran YH
AD  - Institute of Health and Environmental Medicine, Academy of Military Medical 
      Sciences, Beijing, China.
FAU - Wang, Hai
AU  - Wang H
LA  - eng
PT  - Journal Article
PL  - China
TA  - J Zhejiang Univ Sci B
JT  - Journal of Zhejiang University. Science. B
JID - 101236535
RN  - 0 (KATP Channels)
RN  - 0 (N-(1-methylethyl)-1,1,2-trimethylpropylamine)
RN  - 0 (Neuroprotective Agents)
RN  - 0 (Propylamines)
RN  - EC 1.1.1.27 (L-Lactate Dehydrogenase)
SB  - IM
MH  - Animals
MH  - Apoptosis/drug effects
MH  - Brain Edema/drug therapy
MH  - Cerebral Infarction/*drug therapy
MH  - KATP Channels/*drug effects
MH  - L-Lactate Dehydrogenase/metabolism
MH  - Male
MH  - Neuroprotective Agents/*therapeutic use
MH  - Propylamines/*therapeutic use
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Reperfusion Injury/*prevention & control
PMC - PMC3190099
EDAT- 2011/10/01 06:00
MHDA- 2012/02/03 06:00
PMCR- 2011/10/01
CRDT- 2011/10/01 06:00
PHST- 2011/10/01 06:00 [entrez]
PHST- 2011/10/01 06:00 [pubmed]
PHST- 2012/02/03 06:00 [medline]
PHST- 2011/10/01 00:00 [pmc-release]
AID - 10.1631/jzus.B1100067 [doi]
PST - ppublish
SO  - J Zhejiang Univ Sci B. 2011 Oct;12(10):835-45. doi: 10.1631/jzus.B1100067.