抑制AMPK激活对脑缺血小鼠行为学和脑梗死体积的影响  

The Impact of Inhibiting Adenosine Monophosphate Activated Protein Kinase on the Behavior and Cerebral Infarction Volume of Mice after Cerebral Ischemia

作　　者：马毓[1] 党辉[1] 补娟[1] 景燕[1] 李红燕[1] 朱沂[1] 

机构地区：[1]新疆维吾尔自治区人民医院,新疆乌鲁木齐830001

出　　处：《中国医学创新》2016年第28期1-6,共6页Medical Innovation of China

基　　金：新疆维吾尔自治区自然科学基金(2014211A057)

摘　　要：目的:探讨抑制磷酸腺苷活化蛋白激酶(AMPK)激活对脑缺血小鼠行为和脑梗死体积的影响。方法:选取雄性昆明小鼠66只,随机分为假手术组、盐水对照组及药物干预组,每组22只。药物干预组在缺血时腹腔注射AMPK特异性抑制剂Compound C(20 mg/kg),采用线栓法制作大脑中动脉栓塞/再灌注模型,盐水对照组在相同时间给予等量0.9%氯化钠注射液腹腔注射,假手术组不给予任何药物。再灌注24 h后对小鼠进行神经功能评分,TTC染色观察脑梗死体积,Westem-Blot法检测缺血侧大脑中pAMPK蛋白表达。结果:假手术组无神经功能缺损和脑梗死灶,脑组织有少量pAMPK蛋白表达,包括皮质(0.700±0.197)和海马(0.690±0.228);脑缺血再灌注损伤后,盐水对照组小鼠神经功能评分(2.63±0.52)分,脑梗死体积(49.57±9.71)%,缺血侧脑组织pAMPK蛋白包括皮质(1.410±0.322)和海马(1.510±0.418),均较假手术组增高(P<0.05);药物干预组神经功能评分(1.88±0.64)分,脑梗死体积(24.07±7.74)%,缺血侧脑组织中pAMPK蛋白包括皮质(0.930±0.229)和海马(0.960±0.378),均较盐水对照组降低(P<0.05)。结论:小鼠脑缺血再灌注损伤后,缺血侧脑组织中AMPK被激活,抑制AMPK激活具有神经保护作用。Objective： To discuss the impact of inhibiting adenosine monophosphate activated protein kinase （ AMPK ） on the behavior and cerebral infarction volume of mice after cerebral ischemia.Metbod： Sixty- six male Kunming mice were randomly divided into the sham operation group, saline control group and drug intervention group, each group had 22 mice.The AMPK specific inhibitor Compound C （ 20 mg/kg ） was injected intraperitoneally in the drug intervention group during the time of isehemia, the middle cerebral artery occlusion/ reperfusion model was made by thread embolism method, saline control group was given intraperitoneal injection of normal saline at the same time and the sham operation group did not give any drugs.After reperfusion for 24 h, the neurological function score was evaluated in mice, TTC staining was used to observe the volume of cerebral infarction and Westem-Blot method was used to detect the expression of pAMPK protein in the ischemic side of the brain.Result： There were no neurologic impairments and cerebral infarctions in the sham operation group, there was a small amount of pAMPK protein expression includes cortex （ 0.700 ± 0.197 ） and hippocampus （ 0.690 ± 0.228 ） .After cerebral ischemia reperfusion injury, the neurological function score were （ 2.63 ± 0.52 ） in the saline control group, the volume of cerebral infarction was （ 49.57 ± 9.71 ） %, ischemia side brain tissue pAMPK protein includes the cortex （ 1.410± 0.322 ） and the hippocampus （ 1.510 ±0.418 ）, were higher than those of the sham operation group （ P〈0.05 ） .The neurological function scores were （ 1.88 ± 0.64 ） in the drug intervention group, the volume of cerebral infarction was （ 24.07 ± 7.74 ） %, ischemia side brain tissue pAMPK protein includes the cortex （ 0.930 ± 0.229 ） and the hippocampus （ 0.960 ± 0.378 ）, were lower than those of the saline control group （P〈0.05） .Conclusion： After cerebral ischemia reperfusion injury, AMPK is overactivated in

关 键 词：脑缺血再灌注损伤 磷酸腺苷活化蛋白激酶 神经保护 

分 类 号：R743.3[医药卫生—神经病学与精神病学]