rdf:type |
|
lifeskim:mentions |
umls-concept:C0001613,
umls-concept:C0007776,
umls-concept:C0022655,
umls-concept:C0027882,
umls-concept:C0032821,
umls-concept:C0033487,
umls-concept:C0034693,
umls-concept:C0034721,
umls-concept:C0205421,
umls-concept:C0257694,
umls-concept:C0442030,
umls-concept:C0521116,
umls-concept:C1709866,
umls-concept:C1879547
|
pubmed:issue |
1-3
|
pubmed:dateCreated |
2011-1-14
|
pubmed:abstractText |
Propofol has been shown to exert neuroprotective effects. Delayed rectifier potassium current (I(K)) was reported to be closely related to neuronal damage. This study was designed to test the effects of propofol on I(K) in rat parietal cortical neurons and the involvement of PKC in this activity. Whole-cell patch-clamp recordings were performed in rat parietal cortical neurons. The amplitudes of I(K) were recorded before and after the addition of different concentrations of propofol. Propofol concentration-dependently inhibited I(K) with an IC50 value of 36.3±2.7 ?M. Moreover, propofol caused a downward shift of the I-V curve of I(K) in a concentration dependent manner. The kinetics of I(K) was altered by propofol, with decreased activation and delayed recovery of I(K). Pretreatment with calphostin-C (a non-selective inhibitor of PKC) or PKC epsilon translocation inhibitor peptide (PKC epsilon inhibitor) abrogated the inhibition of I(K) by propofol. In conclusion, propofol inhibited I(K) via the activation of PKC epsilon in rat cerebral parietal cortical neurons.
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pubmed:language |
eng
|
pubmed:journal |
|
pubmed:citationSubset |
IM
|
pubmed:chemical |
|
pubmed:status |
MEDLINE
|
pubmed:month |
Feb
|
pubmed:issn |
1879-0712
|
pubmed:author |
pubmed-author:CuiXiao-GuangXG,
pubmed-author:GaoWeiW,
pubmed-author:LiWen-ZhiWZ,
pubmed-author:PanZhen-WeiZW,
pubmed-author:QuLi-HuiLH,
pubmed-author:SongChun-YuCY,
pubmed-author:WarrP BPB,
pubmed-author:XiHong-JieHJ,
pubmed-author:YangLeiL,
pubmed-author:YueZi-YongZY,
pubmed-author:ZhouJinJ
|
pubmed:copyrightInfo |
Copyright © 2010 Published by Elsevier B.V.
|
pubmed:issnType |
Electronic
|
pubmed:day |
25
|
pubmed:volume |
653
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
16-20
|
pubmed:meshHeading |
pubmed-meshheading:21114997-Animals,
pubmed-meshheading:21114997-Delayed Rectifier Potassium Channels,
pubmed-meshheading:21114997-Dose-Response Relationship, Drug,
pubmed-meshheading:21114997-Female,
pubmed-meshheading:21114997-Male,
pubmed-meshheading:21114997-Naphthalenes,
pubmed-meshheading:21114997-Neurons,
pubmed-meshheading:21114997-Neuroprotective Agents,
pubmed-meshheading:21114997-Parietal Lobe,
pubmed-meshheading:21114997-Patch-Clamp Techniques,
pubmed-meshheading:21114997-Propofol,
pubmed-meshheading:21114997-Protein Kinase C-epsilon,
pubmed-meshheading:21114997-Rats,
pubmed-meshheading:21114997-Rats, Wistar
|
pubmed:year |
2011
|
pubmed:articleTitle |
Propofol inhibited the delayed rectifier potassium current (I(k)) via activation of protein kinase C epsilon in rat parietal cortical neurons.
|
pubmed:affiliation |
Department of Anesthesiology, The Second Affiliated Hospital of Harbin Medical University, Harbin, China.
|
pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|