2007Acta Academiae Medicinae XuzhouRequires access

PKCγ contributes to the protective effect of isoflurane against focal cerebral ischemia-reperfusion injury in rats

Zeng Yin-ming

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Abstract

Objective To investigate the relationship between the protective effect of isoflurane preconditioning against focal cerebral ischemia-reperfusion injury and the expression of gamma isoform of protein kinase C(PKCγ) in rats.Methods Twenty-four male SD rats weighing 250-300 g were randomly allocated into sham-operation,ischemia-reperfusion(I/R) and isoflurane preconditioned I/R groups(n=8 each).Using the intraluminal filament technique under chloral hydrate anesthesia,the I/R rats were subjected to 2 hours of middle cerebral artery occlusion(MCAO).To the preconditioning group,1.5% isoflurane inhalation was given for 1 hour before MCAO.Neurological deficit of the rats was assessed by Zea Longa's scoring system(0= no deficit,4=unable to walk and unconscious),infarct size was determined by TTC staining and quantitative image analysis,and the PKCγ protein expression in the frontal lobe of cerebral cortex was evaluated by immunofluorescence,24 hours after reperfusion.Results The neurologic deficit and infarct size in I/R group were significantly higher than in preconditioned I/R group(P0.05).Compared with that in the sham-operation group,the expression of PKCγ in frontal lobe was reduced in the I/R group and increased in the preconditioned I/R group(P0.05).Conclusion One mechanism of the protective effect of isoflurane preconditioning against focal cerebral I/R injury in rats is likely to be the up regulation of PKCγ expression in the frontal lobe of cerebral cortex.

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Objective To investigate the relationship between the protective effect of isoflurane preconditioning against focal cerebral ischemia-reperfusion injury and the expression of gamma isoform of protein kinase C(PKCγ) in rats.Methods Twenty-four male SD rats weighing 250-300 g were randomly allocated into sham-operation,ischemia-reperfusion(I/R) and isoflurane preconditioned I/R groups(n=8 each).Using the intraluminal filament technique under chloral hydrate anesthesia,the I/R rats were subjected to 2 hours of middle cerebral artery occlusion(MCAO).To the preconditioning group,1.5% isoflurane inhalation was given for 1 hour before MCAO.Neurological deficit of the rats was assessed by Zea Longa's scoring system(0= no deficit,4=unable to walk and unconscious),infarct size was determined by TTC staining and quantitative image analysis,and the PKCγ protein expression in the frontal lobe of cerebral cortex was evaluated by immunofluorescence,24 hours after reperfusion.Results The neurologic deficit and infarct size in I/R group were significantly higher than in preconditioned I/R group(P0.05).Compared with that in the sham-operation group,the expression of PKCγ in frontal lobe was reduced in the I/R group and increased in the preconditioned I/R group(P0.05).Conclusion One mechanism of the protective effect of isoflurane preconditioning against focal cerebral I/R injury in rats is likely to be the up regulation of PKCγ expression in the frontal lobe of cerebral cortex.

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Available abstract

Objective To investigate the relationship between the protective effect of isoflurane preconditioning against focal cerebral ischemia-reperfusion injury and the expression of gamma isoform of protein kinase C(PKCγ) in rats.Methods Twenty-four male SD rats weighing 250-300 g were randomly allocated into sham-operation,ischemia-reperfusion(I/R) and isoflurane preconditioned I/R groups(n=8 each).Using the intraluminal filament technique under chloral hydrate anesthesia,the I/R rats were subjected to 2 hours of middle cerebral artery occlusion(MCAO).To the preconditioning group,1.5% isoflurane inhalation was given for 1 hour before MCAO.Neurological deficit of the rats was assessed by Zea Longa's scoring system(0= no deficit,4=unable to walk and unconscious),infarct size was determined by TTC staining and quantitative image analysis,and the PKCγ protein expression in the frontal lobe of cerebral cortex was evaluated by immunofluorescence,24 hours after reperfusion.Results The neurologic deficit and infarct size in I/R group were significantly higher than in preconditioned I/R group(P0.05).Compared with that in the sham-operation group,the expression of PKCγ in frontal lobe was reduced in the I/R group and increased in the preconditioned I/R group(P0.05).Conclusion One mechanism of the protective effect of isoflurane preconditioning against focal cerebral I/R injury in rats is likely to be the up regulation of PKCγ expression in the frontal lobe of cerebral cortex.

Key concepts: Isoflurane, Ischemia, Medicine, Anesthesia, Reperfusion injury, Chloral hydrate, Occlusion, Cerebral cortex

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