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首页> 外文期刊>European Journal of Pharmacology: An International Journal >Propofol inhibited the delayed rectifier potassium current (I(k)) via activation of protein kinase C epsilon in rat parietal cortical neurons.
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Propofol inhibited the delayed rectifier potassium current (I(k)) via activation of protein kinase C epsilon in rat parietal cortical neurons.

机译:丙泊酚通过激活大鼠顶叶皮层神经元中的蛋白激酶Cε抑制延迟的整流钾电流(I(k))。

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摘要

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 muM. 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.
机译:异丙酚已被证明具有神经保护作用。据报道,延迟整流器钾电流(I(K))与神经元损害密切相关。这项研究旨在测试异丙酚对大鼠顶叶皮层神经元中I(K)的影响以及PKC参与这种活动的作用。在大鼠顶叶皮层神经元中进行全细胞膜片钳记录。在添加不同浓度的异丙酚之前和之后记录I(K)的幅度。异丙酚浓度依赖性地抑制I(K),IC50值为36.3 +/- 2.7μM。此外,丙泊酚以浓度依赖性方式引起I(K)的I-V曲线的向下移动。异丙酚改变了I(K)的动力学,降低了I(K)的活化和恢复时间。用calphostin-C(PKC的非选择性抑制剂)或PKC epsilon易位抑制剂肽(PKC epsilon抑制剂)进行的预处理消除了异丙酚对I(K)的抑制作用。总之,丙泊酚通过激活大鼠大脑顶叶皮层神经元中的PKCε抑制了I(K)。

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