2010Journal of Apoplexy and Nervous DiseasesRequires access

Effect of ischemic postconditioning on neuron apoptosis and expression of β-Amyloid protein1-40 in hippocampus CA_1 region following cerebral ischemia/reperfusion in rats

Liu Jia-li

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Abstract

Objective To explore the effect of ischemic postconditioning on neuron apoptosis and expression of β-Amyloid protein 1-40(Aβ1-40)in hippocampus CA1 region following cerebral ischemia/reperfusion(I/R) in rats.Methods Forty male Sprague-Dawley rats were randomly divided into sham-operation(SH) group,I/R group and ischemic postconditioning(IP) group.Using thread embolism method to develop the model of focal cerebral ischemic reperfusion injury in rats.Rats were treated with postconditioning after 60 minutes of occlusion.Neurologic scores,the number of neuron apoptosis in hippocampus CA1 region and expressions of Aβ1-40 were assessed at 24 hours.Results Compared with I/R group,the neurologic scores in IP group decreased significantly(P0.01),the number of apoptosis in hippocampus CA1 region in IP group decreased significantly(P0.01),and the expressions of Aβ1-40 in the ischemic hippocampus CA1 region were upregulated significantly(P0.01).There were significant positive correlations between the neuron apoptosis and expression level of Aβ1-40.Conclusions Those findings indicate that postconditioning inhibits focal cerebral ischemia/reperfusion injury.The expressions of Aβ1-40 do increased after ischemia/reperfusion.Ischemic postconditioning could downregulate the level of Aβ1-40.Its reveals that neuroprotective mechanism of postconditioning may be related with Aβ1-40.

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Objective To explore the effect of ischemic postconditioning on neuron apoptosis and expression of β-Amyloid protein 1-40(Aβ1-40)in hippocampus CA1 region following cerebral ischemia/reperfusion(I/R) in rats.Methods Forty male Sprague-Dawley rats were randomly divided into sham-operation(SH) group,I/R group and ischemic postconditioning(IP) group.Using thread embolism method to develop the model of focal cerebral ischemic reperfusion injury in rats.Rats were treated with postconditioning after 60 minutes of occlusion.Neurologic scores,the number of neuron apoptosis in hippocampus CA1 region and expressions of Aβ1-40 were assessed at 24 hours.Results Compared with I/R group,the neurologic scores in IP group decreased significantly(P0.01),the number of apoptosis in hippocampus CA1 region in IP group decreased significantly(P0.01),and the expressions of Aβ1-40 in the ischemic hippocampus CA1 region were upregulated significantly(P0.01).There were significant positive correlations between the neuron apoptosis and expression level of Aβ1-40.Conclusions Those findings indicate that postconditioning inhibits focal cerebral ischemia/reperfusion injury.The expressions of Aβ1-40 do increased after ischemia/reperfusion.Ischemic postconditioning could downregulate the level of Aβ1-40.Its reveals that neuroprotective mechanism of postconditioning may be related with Aβ1-40.

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Available abstract

Objective To explore the effect of ischemic postconditioning on neuron apoptosis and expression of β-Amyloid protein 1-40(Aβ1-40)in hippocampus CA1 region following cerebral ischemia/reperfusion(I/R) in rats.Methods Forty male Sprague-Dawley rats were randomly divided into sham-operation(SH) group,I/R group and ischemic postconditioning(IP) group.Using thread embolism method to develop the model of focal cerebral ischemic reperfusion injury in rats.Rats were treated with postconditioning after 60 minutes of occlusion.Neurologic scores,the number of neuron apoptosis in hippocampus CA1 region and expressions of Aβ1-40 were assessed at 24 hours.Results Compared with I/R group,the neurologic scores in IP group decreased significantly(P0.01),the number of apoptosis in hippocampus CA1 region in IP group decreased significantly(P0.01),and the expressions of Aβ1-40 in the ischemic hippocampus CA1 region were upregulated significantly(P0.01).There were significant positive correlations between the neuron apoptosis and expression level of Aβ1-40.Conclusions Those findings indicate that postconditioning inhibits focal cerebral ischemia/reperfusion injury.The expressions of Aβ1-40 do increased after ischemia/reperfusion.Ischemic postconditioning could downregulate the level of Aβ1-40.Its reveals that neuroprotective mechanism of postconditioning may be related with Aβ1-40.

Key concepts: Neuroprotection, Hippocampus, Ischemia, Medicine, Apoptosis, Downregulation and upregulation, Neuron, Anesthesia

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Effect of ischemic postconditioning on neuron apoptosis and expression of β-Amyloid protein1-40 in hippocampus CA_1 region following cerebral ischemia/reperfusion in rats — Research Paper | ScholarLens