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K(2)P 通道-TREK1 的激活介导七氟醚预处理诱导的神经保护作用。

Activation of K(2)P channel-TREK1 mediates the neuroprotection induced by sevoflurane preconditioning.

机构信息

Department of Anesthesiology, Xijing Hospital, Xi'an, Shanxi 710032, China.

Department of Anesthesiology, Xijing Hospital, Xi'an, Shanxi 710032, China

出版信息

Br J Anaesth. 2014 Jul;113(1):157-67. doi: 10.1093/bja/aet338. Epub 2013 Oct 22.

DOI:10.1093/bja/aet338
PMID:24154701
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4062297/
Abstract

BACKGROUND

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.

METHODS

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.

RESULTS

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.

CONCLUSIONS

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.

摘要

背景

挥发性麻醉剂预处理可诱导局灶性脑缺血耐受，但其潜在机制尚未明确。本研究分析双孔钾通道 TREK-1 是否在七氟醚介导的神经保护中发挥作用，TREK-1 是双孔域钾（K+）通道，也是挥发性麻醉剂的作用靶点。

方法

用七氟醚对分化的 SH-SY5Y 细胞进行预处理，然后用氧葡萄糖剥夺（OGD）进行挑战。评估细胞活力以及半胱天冬酶-3 和 TREK-1 的表达。用七氟醚预处理大鼠，然后进行大脑中动脉闭塞（MCAO），并分析 TREK-1 蛋白和 mRNA 的表达。评估神经评分和梗死体积。

结果

七氟醚预处理可减少 OGD 刺激的分化 SH-SY5Y 细胞的死亡。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。七氟醚预处理增加 TREK-1 mRNA 和蛋白的水平。TREK-1 敲低显著减弱了体外和体内七氟醚预处理诱导的神经保护作用。

结论

七氟醚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。这些结果提示了七氟醚预处理诱导的局灶性脑缺血耐受的新机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee7c/4062297/851babf30fd6/aet33805.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee7c/4062297/472c39e1fe0b/aet33801.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee7c/4062297/e4a6389c0b96/aet33802.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee7c/4062297/0ee9424b9fbb/aet33803.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee7c/4062297/84ac7a6a82a7/aet33804.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee7c/4062297/851babf30fd6/aet33805.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee7c/4062297/472c39e1fe0b/aet33801.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee7c/4062297/e4a6389c0b96/aet33802.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee7c/4062297/0ee9424b9fbb/aet33803.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee7c/4062297/84ac7a6a82a7/aet33804.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee7c/4062297/851babf30fd6/aet33805.jpg

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