Fig. 5. The inhibition of adenosine 5′-triphosphate–sensitive potassium channel blockers on isoflurane postconditioning (Iso-post)–induced neuroprotection. Corticostriatal slices were subjected to a 15-min oxygen–glucose deprivation (OGD) and then were immediately postconditioned with or without 2% isoflurane for 30 min in the presence or absence of 0.3 μm glibenclamide or 500 μm 5-hydroxydecanoic acid (5-HD). Cell injury was quantified by 2,3,5-triphenyltetrazolium chloride (TTC) conversion 2 h after OGD. Results are mean ± SD (n = 10). Statistical analysis was performed by one-way repeated-measures analysis of variance followed by the Dunn method. *  P < 0.05 compared with OGD only. Gli = glibenclamide. 

Fig. 5. The inhibition of adenosine 5′-triphosphate–sensitive potassium channel blockers on isoflurane postconditioning (Iso-post)–induced neuroprotection. Corticostriatal slices were subjected to a 15-min oxygen–glucose deprivation (OGD) and then were immediately postconditioned with or without 2% isoflurane for 30 min in the presence or absence of 0.3 μm glibenclamide or 500 μm 5-hydroxydecanoic acid (5-HD). Cell injury was quantified by 2,3,5-triphenyltetrazolium chloride (TTC) conversion 2 h after OGD. Results are mean ± SD (n = 10). Statistical analysis was performed by one-way repeated-measures analysis of variance followed by the Dunn method. *  P < 0.05 compared with OGD only. Gli = glibenclamide. 

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