Activation of K(2)P channel-TREK1 mediates the neuroprotection induced by sevoflurane preconditioning.
Activation of K(2)P channel-TREK1 mediates the neuroprotection induced by sevoflurane preconditioning.
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K2P通道-TREK1的激活介导七氟烷预处理诱导的神经保护作用
DOI：
10.1093/bja/aet338
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发表时间：
2014-07
影响因子：
9.8
通讯作者：
Dong H
中科院分区：
文献类型：
--
作者：
Tong L;Cai M;Huang Y;Zhang H;Su B;Li Z;Dong H
挥发性麻醉剂预处理诱导局灶性脑缺血耐受，但其机制尚不清楚。本研究分析了TREK-1（一种双孔结构域K+通道和挥发性麻醉剂的靶点）是否在介导七氟烷的神经保护作用中发挥作用。用七氟醚预处理分化的SH-SY 5 Y细胞，并通过氧糖剥夺（OGD）进行攻击。评价细胞活力以及半胱天冬酶-3和TREK-1的表达。采用七氟醚预处理的大鼠制作大脑中动脉闭塞（MCAO）模型，分析TREK-1蛋白和mRNA的表达。评估神经系统评分并检查梗死体积。七氟烷预处理减少OGD激发的分化SH-SY 5 Y细胞的细胞死亡。七氟醚预处理可减少MCAO大鼠的梗死体积并改善神经功能结局。七氟烷预处理增加TREK-1 mRNA和蛋白水平。在体外和体内，TREK-1的敲低显著减弱了七氟烷预处理诱导的神经保护作用。七氟烷预处理诱导的短暂性脑缺血损伤的神经保护作用涉及TREK-1通道。这些结果提示七氟烷预处理诱导的局灶性脑缺血耐受的新机制。
Preconditioning with volatile anaesthetic agents induces tolerance to focal cerebral ischaemia, although the underlying mechanisms have not been clearly defined. The present study analyses whether TREK-1, a two-pore domain K+ channel and target for volatile anaesthetics, plays a role in mediating neuroprotection by sevoflurane. Differentiated SH-SY5Y cells were preconditioning with sevoflurane and challenged by oxygen–glucose deprivation (OGD). Cell viability and expression of caspase-3 and TREK-1 were evaluated. Rats that were preconditioned with sevoflurane were subjected to middle cerebral artery occlusion (MCAO), and the expression of TREK-1 protein and mRNA was analysed. Neurological scores were evaluated and infarction volume was examined. Sevoflurane preconditioning reduced cell death in differentiated SH-SY5Y cells challenged by OGD. Sevoflurane preconditioning reduced infarct volume and improved neurological outcome in rats subjected to MCAO. Sevoflurane preconditioning increased levels of TREK-1 mRNA and protein. Knockdown of TREK-1 significantly attenuated sevoflurane preconditioning-induced neuroprotective effects in vitro and in vivo. Sevoflurane preconditioning-induced neuroprotective effects against transient cerebral ischaemic injuries involve TREK-1 channels. These results suggest a novel mechanism for sevoflurane preconditioning-induced tolerance to focal cerebral ischaemia.
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影响因子：
3.4
作者：
Cheung, Yuen-Ting;Lau, Way Kwok-Wai;Chang, Raymond Chuen-Chung
通讯作者：
Chang, Raymond Chuen-Chung
影响因子：
5.7
作者：
Harada, H;Kelly, PJ;Patel, PM
通讯作者：
Patel, PM
影响因子：
8.3
作者：
GARCIA, JH;WAGNER, S;HU, XJ
通讯作者：
HU, XJ
影响因子：
82.9
作者：
Hommel, JD;Sears, RM;DiLeone, RJ
通讯作者：
DiLeone, RJ
影响因子：
6.3
作者：
Namiranian, Khodadad;Brink, Christa D.;Bryan, Robert M., Jr.
通讯作者：
Bryan, Robert M., Jr.