Propofol inhibits bERG K+ channels and enhances the inhibition effects on its mutations in HEK293 ce

来源 :2016第十一届心血管药理专业委员会全国心脑血管药理学术会议 | 被引量 : 0次 | 上传用户:mn6543210
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QT prolongation, a potential risk for arrhythmias, may result from the polymorphism of genes relevant to heart cell repolarization.Another noted cause of QT prolongation is administration of chemical compounds, such as anesthetics, which may affect a specific type of cardiac K+ channel encoded by human ether-a-go-go-related gene (hERG).hERG K+ current was recorded using whole-cell patch clamp in HEK293 cells expressing wild type or mutated hERG gene.Expression of the hERG K+ channel proteins was evaluated with Western blot and then confirmed by fluorescent staining and imaging.Computational modeling was adopted to seek the possible combining site(s) of propofol to hERG K+ channel molecules.
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