CAJ | 학술논문

目的探讨抑制磷酸腺苷活化蛋白激酶(AMPK)活性对小鼠脑缺血再灌注损伤后神经功能评分、脑梗死体积及神经元凋亡的影响. 方法 72只雄性C57BL/6小鼠按随机数字表法分为假手术组、缺血再灌注组、缺血再灌注治疗组,每组24只.后两组采用线栓法建立小鼠大脑中动脉闭塞(MCAO)模型,其中缺血再灌注治疗组在插入线栓时腹腔注射AMPK抑制剂Compound C,缺血再灌注组于同等时间给予等量生理盐水腹腔注射.在小鼠脑缺血再灌注损伤后24 h,采用Longa法测定各组大鼠神经功能缺损评分,采用2,3,5-三苯基氯化四氮唑(TTC)染色测量脑梗死体积,采用TUNEL染色法观察神经元凋亡情况. 结果与缺血再灌注组相比[(2.10±0.24)分;43.10％±11.50％;皮质:(81.00±12.21)个/视野,海马:(56.00±5.29)个/视野]相比,缺血再灌注治疗组神经功能缺损评分[(1.58±0.22)分]、脑梗死体积(24.84％±12.53％)及神经元凋亡数量[皮质:(58.86±9.65)个/视野,海马:(43.33±3.79)个/视野]均明显减少,差异均有统计学意义(P＜0.05). 结论抑制AMPK活性能减少小鼠脑缺血再灌注损伤后的神经元凋亡,具有神经保护作用.
목적 탐토억제린산선감활화단백격매(AMPK)활성대소서뇌결혈재관주손상후신경공능평분、뇌경사체적급신경원조망적영향. 방법 72지웅성C57BL/6소서안수궤수자표법분위가수술조、결혈재관주조、결혈재관주치료조,매조24지.후량조채용선전법건립소서대뇌중동맥폐새(MCAO)모형,기중결혈재관주치료조재삽입선전시복강주사AMPK억제제Compound C,결혈재관주조우동등시간급여등량생리염수복강주사.재소서뇌결혈재관주손상후24 h,채용Longa법측정각조대서신경공능결손평분,채용2,3,5-삼분기록화사담서(TTC)염색측량뇌경사체적,채용TUNEL염색법관찰신경원조망정황. 결과 여결혈재관주조상비[(2.10±0.24)분;43.10％±11.50％;피질:(81.00±12.21)개/시야,해마:(56.00±5.29)개/시야]상비,결혈재관주치료조신경공능결손평분[(1.58±0.22)분]、뇌경사체적(24.84％±12.53％)급신경원조망수량[피질:(58.86±9.65)개/시야,해마:(43.33±3.79)개/시야]균명현감소,차이균유통계학의의(P＜0.05). 결론 억제AMPK활성능감소소서뇌결혈재관주손상후적신경원조망,구유신경보호작용.
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.