东莨菪碱诱导的阿尔茨海默型痴呆大鼠胆碱缺乏条件下血管损伤的作用

G. Gubina-Vakulik, Y. Zorenko
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摘要

背景。胆碱缺乏与血管功能障碍之间的关系继续与阿尔茨海默病的研究相关。目标。研究东莨菪碱诱导的阿尔茨海默型痴呆大鼠胆碱缺乏状态下血管损伤的形态学特征。方法。实验以48只体重180-230克的WAG种群雄性大鼠为实验对象。在第14天和第28天,分别以1 mg/kg体重腹腔注射scopi -14-SC、scopi -28、scopi -28-SC组大鼠,并以每只大鼠50万个细胞的单次剂量静脉注射间充质干细胞(SC)。对照组动物(gr.C)注射0.9%氯化钠。用刚果红和没食子菁铬明矾染色,按照艾纳逊总核酸法。免疫组化法检测脑组织细胞质中VEGF、E-cadherin的表达。结果。实验组动脉壁呈嗜嗜性染色,内皮细胞减少,E-cadherin表达低,毛细血管壁周细胞数量增加。VEGF在内皮细胞、海马神经元中的表达高于gr. scope -14。它表明血管生成和乙酰胆碱合成的激活更强烈,相应的血管损伤和胆碱缺乏更明显。缺氧反应下皮质神经元胞质弥漫性标记VEGF抗体,但表达水平与gr.C无明显差异。在所有组中,根据Einarson染色,大半球神经堆的光密度降低,即神经元过程中的RNA水平降低。由于内皮细胞年轻,干细胞的引入恢复了毛细血管壁,减少了所有研究细胞中VEFG的合成,增加了神经元过程中的RNA含量。结论。胆碱缺乏与神经元过程丧失和血管损伤之间的关系已被发现。血管的自我修复是通过替代的方式进行的,在干细胞引入后,通过修复。
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The role of vascular injury within the conditions of choline deficiency in rats with scopolamine-induced alzheimer's type dementia
Background. The relationship between choline deficiency and vascular dysfunction continues to be relevant in the study of Alzheimer's disease. Objective. To study the morphological characteristics of vascular injury within the conditions of choline deficiency in rats with scopolamine-induced Alzheimer's type dementia. Methods. The experiment was performed on 48 WAG population male rats weighing 180-230 gr. Rats from groups Scop-14, Scop-14-SC, Scop-28, Scop-28-SC were injected intraperitoneally with scopolamine (Scop) butylbromide at a dosage of 1 mg/kg of body mass during 14 and 28 days and intravenously with mesenchymal stem cells (SC) at a single dosage of 500000 cells per 1 rat. Control animals (gr.C) were injected with 0.9% sodium chloride. Brain slides were stained with Congo-red and gallocyanine-chromium alum according to Einarson's method for total nucleic acids. The VEGF, E-cadherin expression was immunohistochemically determined in the brain cells cytoplasm. Results. The congophilic staining of the arteries walls, a decrease in endothelial cells with low the E-cadherin expression and an increase in the number of pericytes in the capillary wall was observed in the experimental groups. In gr.Scop-28 VEGF expression in endothelial cells, hippocampal neurons was greater than in gr.Scop-14. It indicated more intensive activation of angiogenesis and acetylcholine synthesis with correspondingly more pronounced vascular damage and choline deficiency. The cytoplasm of cortical neurons was diffusely labeled with VEGF antibodies in response to hypoxia, but the level of expression was almost no different from that in gr.C. In all groups, the optical density of the neuropile of the large hemispheres according to Einarson’s staining was reduced, i.e., the level of RNA in the neuronal processes was reduced. The introduction of stem cells restored the capillary wall due to young endothelial cells, reduced the VEFG synthesis in all studied cells and increased the RNA content in neuronal processes. Conclusion. The relationship between choline deficiency, neuronal process loss and vascular damage has been found. The blood vessels self-repair was occurred by substitution, after the stem cells introduction - by restitution.
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