Lithium Chloride Inhibited Neuronal Apoptosis and Glycogen Synthase Kinase -3β Activities in Hippocampal CA1 Area After Middle Cerebral Artery Occlusion and Reperfusion in Rats
Lithium Chloride Inhibited Neuronal Apoptosis and Glycogen Synthase Kinase -3β Activities in Hippocampal CA1 Area After Middle Cerebral Artery Occlusion and Reperfusion in Rats作者机构：Department of Anesthesiology The First Affiliated Hospital of Nanjing Medical University Nanjing 210029 China
出 版 物：《麻醉与监护论坛》 (Forum of Anesthesia and Monitoring)
年 卷 期：2011年第18卷第1期
页 面：43-48页
学科分类：0710[理学-生物学] 07[理学] 071006[理学-神经生物学]
摘 要：Background: Lithium pretreatment has been proved to be neuro-protective. Post-ischemia conditioning attracted more and more attention during the last years. This study was designed to observe the effect of lithium post-treatment on neuron apoptosis and glycogen synthase kinase(GSK)-3βin rats after middle cerebral artery occlusion(MCAO). Methods: The right middle cerebral artery was occluded with a nylon suture for 90 mins. Rats were randomly divided into NO group, SH group, IR group, Lil group (lmmol/kg) , Li2 group (2mmol/kg) , and Li3 group (3mmol/kg) . Animals in each group were killed 6 hours, 1 day, 3day, or 7days after cerebral ischemia, with six rats in each time point. Neuron apoptosis in the CA 1 region were examined by Hoechst staining. The expression and distribution of GSK-3βand p-GSK-3β(Ser9) was examined by immunofluorescence analysis. Results: The apoptotic nuclei was detected significantly in IR groups compared with SH group(P0.01). The amounts of P-GSK-3β(Ser9) seemed increased with the time and they were higher in IR groups than those in SH groups (P0.01). Lithium post-treatment reinforced this tendency dose-dependently (P0.01).Conclusion: Lithium chloride can dose-dependently (1 -3 mmol/kg) suppress neuron apoptosis and GSK-3βafler MCAO/reperfusion injury.
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