Duplicate preconditioning with sevoflurane in vitro improves neuroprotection in rat brain via activating the extracellular signal-regulated protein kinase

Abstract

Abstract:Objective Sevoflurane preconditioning has been demonstrated to reduce cerebral ischemia-reperfusion (IR) injury, but the underlying mechanisms have not been fully elucidated. Besides, different protocols would usually lead to different results. The objective of this study was to determine whether dual exposure to sevoflurane improves the effect of anesthetic preconditioning against oxygen and glucose deprivation (OGD) injury in vitro. Methods Rat hippocampal slices under normoxic conditions (95% O 2 /5% CO 2 ) were pre-exposed to sevoflurane 1, 2 and 3 minimum alveolar concentration (MAC) for 30 min, once or twice, with 15-min washout after each exposure. The slices were then subjected to 13-min OGD treatment (95% N 2 /5% CO 2 , glucose-free), followed by 30-min reoxygenation. The population spikes (PSs) were recorded in the CA1 region of rat hippocampus. The percentage of PS amplitude at the end of 30-min reoxygenation to that before OGD treatment was calculated, since it could indicate the recovery degree of neuronal function. In addition, to assess the role of mitogen-activated protein kinases (MAPKs) in preconditioning, U0126, an inhibitor of extracellular signal-regulated protein kinase (MEK-ERK1/2, ERK1/2 MAPK), and SB203580, an inhibitor of p38 MAPK, were separately added 10 min before sevoflurane exposure. Results Preconditioning once with sevoflurane 1, 2, and 3 MAC increased the percentage of PS amplitude at the end of 30-min reoxygenation to that before OGD treatment, from (15.13±3.79)% (control) to (31.88±5.36)%, (44.00±5.01)%, and (49.50±6.25)%, respectively, and twice preconditioning with sevoflurane 1, 2, and 3 MAC increased the percentage to (38.53±4.36)%, (50.74±7.05)% and (55.86±6.23)%, respectively. The effect of duplicate preconditioning with sevoflurane 3 MAC was blocked by U0126 [(16.23±4.62)%]. Conclusion Sevoflurane preconditioning can induce neuroprotection against OGD injury in vitro, and preconditioning twice enhances this effect. Besides, the activation of extracellular signal-regulated protein kinase (MEK-ERK1/2, ERK1/2 MAPK) may be involved in this process.

Activation of Canonical Notch Signaling Pathway Is Involved in the Ischemic Tolerance Induced by Sevoflurane Preconditioning in Mice

“…Tolerance to brain ischemia induced by sevoflurane preconditioning has been observed in both in vivo and in vitro models. 1,4,23 This study further verified that pretreatment with sevoflurane (2.5%) could induce effective neuroprotection in mice as evidenced by infarct volumes and neurologic behavior scores.…”

Preconditioning with sevoflurane ameliorates spatial learning and memory deficit after focal cerebral ischemia–reperfusion in rats

“…However, the mechanism of sevoflurane preconditioning on neuroprotection is very complex. It occurs through complex signal transduction pathways that involve activation of canonical Notch signaling pathway (Yang et al, 2012), protein kinase C (Ye et al, 2012b), protein kinase Mζ (Wang et al, 2012), tyrosine kinase (Sigaut et al, 2009), extracellular signal‐regulated protein kinase (MEK‐ERK1/2, ERK1/2 MAPK) (Wang et al, 2010), mitochondrial (mito) adenosine troposphere‐regulated potassium (K ATP ) channels (Adamczyk et al, 2010). Furthermore, the neuroprotection of sevoflurane preconditioning involves modification of glutamate transporter activity (Wang et al, 2007a), altering the electrophysiological changes (Wang et al, 2007b), inhibition of mitochondrial pore permeability transition opening (Ye et al, 2012a), releasing reactive oxygen species (Yang et al, 2011), inhibition of inflammation, cerebral lipid peroxidation (Nurdan Bedirli et al, 2012) and apoptosis (Codaccioni et al, 2009; Nurdan Bedirli et al, 2012) of the neurons.…”

Kinin-B2 receptor exerted neuroprotection after diisopropylfluorophosphate-induced neuronal damage

“…Measuring population spike (PS) recovery of pyramidal neurons in hippocampal slices is an accepted in vitro model for measuring physiological parameters, neurotoxicity, and subsequent neuroprotective features of diverse compounds (Wang et al, 2010; Kanak et al, 2011;Ferchmin et al, 2005 Ferchmin et al, 2013). Indeed, recovery of PS activity to similar values, as observed in control measurements in the absence of any drug, was also achieved by blocking apoptosis with caspase-9 or AKT-Glycogen synthase kinase inhibitor (Martins et al 2012).…”