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Effect Of Compound C On AMP-activated Protein Kinase On Neuronal Apoptosis Of Aged Mice After Cerebral Ischemia-reperfusion

Posted on:2016-02-07Degree:MasterType:Thesis
Country:ChinaCandidate:B LiuFull Text:PDF
GTID:2284330470462570Subject:Anesthesia
Abstract/Summary:PDF Full Text Request
Objective To observed the effect of Compound C on the AMP- activated protein kinase(AMPK) in hippocampus,and to evaluate the effects on the apoptosis in hippocampal neurons and expression of apoptosis related-proteins in aged mice after cerebral ischemia-reperfusion.Methods Ninty-six male C57BL6 aged mice were randomly divided into three groups(n=36): Sham-operation group,I/R group and the I/R drug-treatment group. The forebrain ischemia was produced by 15 min transient occlusion of bilateral common carotid artery followed by reperfusion. Aged mice of I/R drug-treatment were injected intraperitoneally with the AMPK inhibitor Compound C at the onset of BCCAO; the same volume was given to I/R group at the same time.On 4h and 48 h of reperfusion, the mice were sacrificed and the brain were immediately harvested for morphological examination of hippocampal and cortical neurons(HE) 、 detection of apoptotic neurons(TUNEL) and determination of p AMPKα、caspase-3 protein expression with Western blot.Results The amount of apoptotic neurons and the number of protein caspase-3 、p-AMPK significantly increased in the I/R and I/R drug treatment versus the sham-operation group on 48h(P<0.05).And the level of p AMPK significantly decreased(P<0.05) but the amount of apoptotic neurons and the number of caspase-3 didn’t have evidently change in the I/R drug treatment group versus the I/R group(P>0.05).Conclusion Inhibition of AMP-activated protein kinase Compound C has non-neuroprotection on aged mice after cerebral ischemia-reperfusion.
Keywords/Search Tags:AMPK, Inhibitor, Reperfusion injury, Brain, Aged, Apoptpsis
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