• Br J Anaesth · Jul 2014

    Activation of K2P channel-TREK1 mediates the neuroprotection induced by sevoflurane preconditioning.

    • L Tong, M Cai, Y Huang, H Zhang, B Su, Z Li, and H Dong.
    • Department of Anesthesiology, Xijing Hospital, Xi'an, Shanxi 710032, China.
    • Br J Anaesth. 2014 Jul 1;113(1):157-67.

    BackgroundPreconditioning 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.MethodsDifferentiated 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.ResultsSevoflurane 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.ConclusionsSevoflurane 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.© The Author [2013]. Published by Oxford University Press on behalf of the British Journal of Anaesthesia.

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