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目的观察人脑缺血后淀粉样β蛋白140(Aβ140)与其淀粉样β蛋白前体(βAPP)在海马CA1区神经元的表达。方法收集43例因脑缺血而梗死的尸检标本,按缺血时间(发病至死亡时间)分为缺血2～6h、7～24h、25～48h、49～72h、73～96h、97～144h组和145～168h组。选取因其他疾病死亡(非脑缺血)尸检标本2例为对照组。采用HE染色方法观察神经细胞损伤情况;免疫组织化学染色检测Aβ140与βAPP在海马CA1区神经元的表达,在镜下对免疫组织化学染色阳性细胞计数,实验结果应用SPSS11.5统计软件进行分析。结果与对照组(2.88个±0.18个/高倍视野)相比,缺血2～6h组Aβ140表达增加(22.44个±2.79个/高倍视野),在73～96h达高峰(36.30个±2.67个/高倍视野),以后有所回落,但仍高于对照组。缺血7～24h组βAPP阳性细胞数量(28.11个±2.03个/高倍视野)显著低于2～6h组(33.30个±0.42个/高倍视野),缺血24h后阳性细胞数量增多,73～96h组达高峰(32.32个±1.36个/高倍视野),96h以后下降,但仍高于对照组(25.90个±1.55个/高倍视野)。24h后βAPP的增加与Aβ140的增加呈显著正相关。结论人脑缺血后Aβ表达增加,并与βAPP协同加重脑缺血性损伤。
Objective To observe the expression of amyloid protein-140 (Aβ140) and its amyloid β-protein precursor (βAPP) in hippocampal CA1 neurons after focal cerebral ischemia in human. Methods 43 autopsy specimens collected from cerebral infarction due to cerebral ischemia were collected and divided into 2 ~ 6h, 7 ~ 24h, 25 ~ 48h, 49 ~ 72h, 73 ~ 96h, 97 ~ 144h group and 145 ~ 168h group. Two other dead necrosis (non-cerebral ischemia) autopsy specimens were selected as the control group. The injury of nerve cells was observed by HE staining. The expression of Aβ140 and βAPP in hippocampal CA1 neurons was detected by immunohistochemical staining. The number of immunohistochemical staining cells was counted by microscopy. The results were analyzed by SPSS11.5 statistical software. Results Compared with control group (2.88 ± 0.18 / high power field), the expression of Aβ140 increased (22.44 ± 2.79 high power fields) at 2 ~ 6h and peaked at 73 ~ 96h (36.30 ± 2.67 / High power field), after falling back, but still higher than the control group. The number of βAPP positive cells (28.11 ± 2.03 / high power field) in 7 ~ 24h group was significantly lower than that in 2 ~ 6h group (33.30 ± 0.42 / high power field), the number of positive cells increased after 24h of ischemia, (32.32 +/- 1.36 high power fields) and decreased after 96 hours, but still higher than the control group (25.90 +/- 1.55 high power fields). After 24h, the increase of βAPP was positively correlated with the increase of Aβ140. Conclusion The expression of Aβ increases after cerebral ischemia, and aggravates cerebral ischemic injury in combination with βAPP.