缺血性脑损伤中HSP72对神经元保护作用的实验研究  

Study on the neuroprotection of HSP72 during brain injury induced by ischemia

作　　者：张芳[1] 刘红芝[1] 张兆成 宋远见[1] 

机构地区：[1]徐州医学院基础学院,221004 [2]徐州市区中小学生卫生保健所

出　　处：《中国实用医药》2009年第4期1-2,共2页China Practical Medicine

基　　金：国家自然科学基金资助(项目编号:30800446);江苏省徐州市科技攻关项目资助(项目编号:xzzd0711)

摘　　要：目的探讨缺血性脑损伤中HSP72对大鼠神经元的保护作用及其分子机制。方法将SD大鼠随机分为假手术组、缺血再灌注对照组、热休克处理组、HSP72反义寡核苷酸组及溶剂组。采用焦油紫染色、免疫印迹检测大鼠缺血再灌注后海马神经元损伤和脑组织AKT、Bad(Ser136)的磷酸化情况。结果热休克处理组与缺血再灌注对照组、HSP72反义寡核苷酸组和溶剂组相比海马神经元损伤减轻,脑组织AKT和Bad(Ser136)磷酸化升高(P<0.05)。结论HSP72可能通过升高脑组织中AKT和Bad(Ser136)的磷酸化程度起到海马神经元保护作用。Objective To investigate the molecular mechanism of neuroprotection of HSP72 during Brain injury induced by ischemia.Methods SD rats were divided randomly into 5 groups：sham-operated;cerebral ischemia and reperfusion;cerebral ischemia and reperfusion＋heat shock treatment;cerebral ischemia and reperfusion＋antisense oligonucleotides and reperfusion＋solvent.Brain injury in hippocampus of rats and change of phosphorylation of AKT and bad（ser 136）were detected by cresly violet-strained or immunoblot assay.Results Comparing with cerebral ischemia and reperfusion group,antisense oligonucleotides and solvent group,the brain injury and phosphorylation of AKT and bad（ser 136） of heat shock treatment team increased significantly.Conclusion HSP72 protected the neurons in hippocampus from ischemia by increasing phosphorylation of AKT and bad（ser 136）.

关 键 词：缺血性脑损伤 HSP72 AKT Bad(Ser136) 

分 类 号：R741[医药卫生—神经病学与精神病学]