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TREK-1 mediates isoflurane-induced cytotoxicity in astrocytes.

Abstract：

BACKGROUND:There are growing concerns that anaesthetic exposure can cause extensive apoptotic degeneration of neurons and the impairment of normal synaptic development and remodelling. However, little attention has been paid to exploring the possible cytotoxicity of inhalation anaesthetics, such as isoflurane, in astrocytes. In this research, we determined that prolonged exposure to an inhalation anaesthetic caused cytotoxicity in astrocytes, and we identified the underlying molecular mechanism responsible for this process. METHODS:Astrocytes were exposed to isoflurane, and astrocytic survival was then measured via LDH release assays, MTT assays, and TUNEL staining. TWIK-related potassium (K+) channel-1 (TREK-1) over-expression and knockdown models were also created using lentiviruses. The levels of TREK-1 and brain-derived neurotrophic factor (BDNF) were measured via Western blot and qRT-PCR. RESULTS:Prolonged exposure to isoflurane decreased primary astrocytic viability in a dose- and time-dependent manner. Moreover, with prolonged exposure to isoflurane, the TREK-1 level increased, and the BDNF level was reduced. TREK-1 knockdown promoted the survival of astrocytes and increased BDNF expression following isoflurane exposure. CONCLUSIONS:Overdoses of and prolonged exposure to isoflurane induce cytotoxicity in primary astrocytes. TREK-1 plays an important role in isoflurane-induced cultured astrocytic cytotoxicity by down-regulating the expression of BDNF.

journal_name

BMC Anesthesiol

journal_title

BMC anesthesiology

authors

Guo H,Peng Z,Yang L,Liu X,Xie Y,Cai Y,Xiong L,Zeng Y

doi

10.1186/s12871-017-0420-5

subject

Has Abstract

pub_date

2017-09-05 00:00:00

pages

124

issue

1

issn

1471-2253

pii

10.1186/s12871-017-0420-5

journal_volume

17

pub_type

杂志文章

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