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- 2018
蛛网膜下腔出血大鼠海马区A-β蛋白表达与认知功能障碍的关联研究
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Abstract:
摘要：目的 研究蛛网膜下腔出血(subarachnoid hemorrhage, SAH)后海马区A-β蛋白表达增加对大鼠学习及记忆功能的影响。方法 将48只SD大鼠随机分为模型组和假手术组，每组24只。采用Bederson法建立SAH模型，分别于造模后第3、7、14、28天时采用Morris水迷宫检测大鼠空间学习及记忆功能，并用免疫组化法检测海马区A-β蛋白的表达。结果 造模后相应时间点，模型组比假手术组逃避潜伏期时间明显延长(P<0.05 )；模型组与假手术组在3d时A-β蛋白表达无明显差异(P>0.05)，在7、14、28d时，A-β阳性细胞计数明显增加(P<0.05)。结论 大鼠SAH后出现学习记忆功能减退及A-β蛋白表达增加，可能促使认知功能障碍的发生。
ABSTRACT: Objective To study the effect of increased brain edema and the expression of A-β protein in the hippocampus on learning and memory functions of rats after subarachnoid hemorrhage (SAH). Methods We randomly divided 48 adult SD rats into model group and sham-operation group, each with 24. The model of SAH was established by Bederson method. Morris water maze was used to detect the spatial learning and memory functions of the rats at day 3, 7, 14 and 28 after modeling; A-β protein expression in the hippocampus was detected by the immunohistochemical method. Results At the corresponding time points after modeling, the latency of escape was significantly longer in model group than that in sham-operation group (P<0.05). However, the two groups did not significantly differ in A-β protein expression at day 3 (P>0.05); A-β positive cell counts increased significantly at days 7, 14 and 28 (P<0.05). Conclusion Memory impairment of learning machine, edema of brain tissue, and the increase of A-β protein expression may induce cognitive dysfunction after SAH
| [1] | MOHAMED S, RIVA R, CONTIN M. Simple and validated UHPLC-MS/MS analysis of nimodipine in plasma and cerebrospinal fluid of patients with subarachnoid haemorrhage[J]. J Chromatogr B Analyt Technol Biomed Life Sci, |
| [2] | 2016, 1028:94-99. |
| [3] | BOERBOOM W, HEIJENBROK-KAL MH, KHAJEH L, et al. Differences in cognitive and emotional outcomes between patients with perimesencephalic and aneurysmal subarachnoid haemorrhage[J]. J Rehabil Med, 2014, 46(1):28-32. |
| [4] | ZHU B, JIANG L, HUANG T, et al. ER-associated degradation regulates Alzheimer’s amyloid pathology and memory function by modulating γ-secretase activity[J]. Nat Commun, 2017, 8(1):1472-1488. |
| [5] | OTITE F, MINK S, TAN CO, et al. Impaired cerebral autoregulation is associated with vasospasm and delayed cerebral ischemia in subarachnoid hemorrhage[J]. Stroke, 2014, 45(3):677-682. |
| [6] | NYBERG C, KARLSSON T, HILLERED L, et al.Metabolic pattern of the acute phase of subarachnoid hemorrhage in a novel porcine model: Studies with cerebral microdialysis with high temporal resolution[J]. PLoS One, 2014, 9(6):e99904. |
| [7] | VAN BEEK AH, CLAASSEN JA. The cerebrovascular role of the cholinergic neural system in Alzheimer’s disease[J]. Behav Brain Res, 2011, 221(2):37-42. |
| [8] | ROWLAND MJ, HADJIPAVLOU G, KELLY M et al. Delayed cerebral ischaemia after subarachnoid haemorrhage: Looking beyond vasospasm[J]. Br J Anaesth, 2012,109(3):315-329. |
| [9] | MAMM AP, SCODELLER, HUSSAIN S. Identification of a peptide recognizing cerebrovascular changes in mouse models of Alzheimer’s disease[J]. Nat Commun, 2017, 8(1):1403-1414. |
| [10] | MAYOR S. Earlier diagnosis is needed to reduce deaths and disability from aneurysmal subarachnoid haemorrhage[J]. BMJ, 2013, 347:6925. |
| [11] | HANSON JE, PARE JF, DENG L, et al. Altered Glun2B NMDA receptor function and synaptic plasticity during early pathology in the PS2APP mouse model of Alzheimer’s disease[J]. Neurobiol, 2015, 74:254-262. |
| [12] | MOTA SI, FERREIRA IL, REGO AC. Dysfunctional synapse in Alzheimer’s disease― A focus on NMDA receptor[J]. Neuropharmacology, 2014, 76:16-26. |
