Abstract
Isoflurane preconditioning could reduce different kinds of brain injury via sphingosine kinase (SPK). Both sphingosine kinase 1 and sphingosine kinase 2 play important roles in brain protection. However, the effects of isoflurane preconditioning on SPK expression in hypertension have not been investigated before. To verify whether the neuroprotective effects of the anesthetic isoflurane after an ischemic injury are altered in hypertension and to identify its possible mechanisms involving SPK. Wistar rats (control) and spontaneous hypertension rats (SHR) were exposed to isoflurane preconditioning before transient middle cerebral artery occlusion. The infarct volumes of cortical and subcortical brain areas were measured. The expression levels of SPK1 and SPK2 were measured before and after isoflurane preconditioning. In the SHR group, isoflurane preconditioning significantly reduced only the infarct volumes of the subcortical brain (p < 0.05), not of the cortical brain. After 3 h of isoflurane exposure and preconditioning, SPK2 levels in the SHR group increased in the cortical brain (p < 0.05), but not in the subcortical brain area, Unlike in the control group, isoflurane exposure and preconditioning could significantly increase SPK2 levels in both cortical and subcortical brain area. The brain protection effects induced by isoflurane preconditioning after an ischemic injury are mainly mediated by the SPK2 isoform and are somewhat impaired in hypertension. Attention should be paid to ischemic injury patients with hypertension.
Highlights
Cerebral preconditioning is a procedure by which a noxious stimulus below the threshold of damage, such as hypoxia, isoflurane and pro-inflammatory cytokines, is applied to the brain in order to induce tolerance to it or to a different noxious stimulus.[1,2] Isoflurane, one of the anesthetics which is typically inhaled, is widely used in various surgical procedures
The brain protection effects induced by isoflurane preconditioning after an ischemic injury are mainly mediated by the SPK2 isoform and are somewhat impaired in hypertension
Determination of cerebral infarct volume in spontaneous hypertension rats (SHR) rats pretreated with isoflurane In the SHR group, trihenylterzolium chloride (TTC) staining analysis revealed that isoflurane preconditioning significantly reduced the infarct volumes of the subcortical brain areas (62.9 ±5.3 mm[3] vs 43.1 ±5.6 mm[3]; p < 0.05; Fig. 1B) but not the cortical brain areas (131.8 ±7.2 mm[3] vs 129.9 ±6.1 mm[3]; Fig. 1B)
Summary
Cerebral preconditioning is a procedure by which a noxious stimulus below the threshold of damage, such as hypoxia, isoflurane and pro-inflammatory cytokines, is applied to the brain in order to induce tolerance to it or to a different noxious stimulus.[1,2] Isoflurane, one of the anesthetics which is typically inhaled, is widely used in various surgical procedures. The sphingosine1-phosphate (S1P) receptor is widely distributed throughout the nervous system It mediates multiple cellular processes, including proliferation, apoptosis and migration, and is regulated by the expression of sphingosine kinase (SPK).[4]. Studies have found that isoflurane could reduce different kinds of brain injury, including both hypoxic ischemia and hemorrhage, in rats through S1P-related pathway.[5,6]. In hypoxic ischemic cerebral damage, Lai et al found a similar result – that isoflurane preconditioning could elevate tolerance levels, mediated by the overexpression of SPK2.9 Both SPK1 and SPK2 play important roles in brain protection. Isoflurane preconditioning could reduce different kinds of brain injury via sphingosine kinase (SPK). Both sphingosine kinase 1 and sphingosine kinase 2 play important roles in brain protection. The effects of isoflurane preconditioning on SPK expression in hypertension have not been investigated before
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