Activation of K2P channel–TREK1 mediates the neuroprotection induced by sevoflurane preconditioning
TLDR
A novel mechanism for sevoflurane preconditioning-induced tolerance to focal cerebral ischaemia is suggested and involved TREK-1 channels, a two-pore domain K+ channel and target for volatile anaesthetics, in vitro and in vivo.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.read more
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Role of TREK-1 in Health and Disease, Focus on the Central Nervous System.
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Amanda Patel,Eric Honoré,François Maingret,Florian Lesage,Michel Fink,Fabrice Duprat,Michel Lazdunski +6 more
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