Abstract

Objective To observe the effect of inhibition of AMP-activated protein kinase (AMPK) activity on neurological deficits,infarct volumes and neuronal apoptosis after cerebral ischemia reperfusion injury in mice.Methods Seventy-two male C57BL/6 mice were randomly divided into three groups (n=24):the sham-operated group,the ischemia reperfusion group and the ischemia reperfusion+treatment group.Mice models of middle cerebral artery occlusion (MCAO) were established by insertion of a thread through internal carotid artery.AMPK inhibitor Compound C was injected intraperitoneally in the mice of ischemia reperfusion+treatment group when the thread was inserted; the same volume of saline was given to ischemia reperfusion group at the same time.Twenty-four h after cerebral ischemia reperfusion,neurological deficits were observed by Longa method; infarct volumes were measured by TTC staining and neuron apoptosis was observed by TUNEL.Results there was a significant reduction in ischemia reperfusion+treatment group in terms of neurological deficits ([1.58±0.22] points vs.[2.10±0.24] points) and infarct volume of ischemia (24.84%±12.53% vs.43.10%± 11.50%) and cell number of neuron apoptosis (cortex:[58.86±9.65]/field vs.[81.00±12.21]/field;hippocampus:[43.33 ±3.79)]/field vs.[56.00±5.29]/field) as compared with ischemia reperfusion group (P<0.05).Conclusion Inhibition of AMPK activity may reduce neuron apoptosis,having neuro-protective role. Key words: Ischemia reperfusion; AMP-actives protein kinase; Neuronal apoptosis; Neuro-protection

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