作　　者： (）;

机构地区： 广东省珠海市第二人民医院神经内科广东珠海519000

出　　处： 《广东医科大学学报》 2018年第4期356-359,共4页

摘　　要： 目的研究Galectin-3在促进阿尔茨海默病发生及病理进展中β淀粉样前体蛋白沉积产生中的作用。方法实验小鼠分为生理盐水组、Galectin-3组、Galectin-3+TD139组,通过Morris水迷宫实验和空间探索实验检测长期Galectin-3处理后小鼠的记忆能力(逃避潜伏期)和学习能力(跨越平台次数),通过免疫荧光检测小鼠大脑内Aβ淀粉样前体蛋白沉积斑块的产生。结果 Galectin-3组小鼠的记忆能力和学习能力较其他两组明显降低(均P<0.05);Galectin-3组中β淀粉样前体蛋白沉积斑块的面积明显大于生理盐水组、Galectin-3+TD139组增大(均P<0.01),而生理盐水组、Galectin-3+TD139组间差异无统计学意义(P>0.05)。结论 Galectin-3在阿尔茨海默病小鼠的病理进展中有重要的作用,Galectin-3能够导致小鼠出现阿尔茨海默病样的学习及记忆能力的下降,并且促进Aβ淀粉样前体蛋白沉积斑块的生成,通过拮抗性抑制剂TD139的使用能够延缓该疾病病理进展。 Objective To explore the effect of Galectin-3 in promoting the generation of plaques of β-amyloid precursor protein during the occurrence and pathology progress of Alzheimer’s disease in mice. Methods The mice were divided into three groups based on different management methods： Group Normal Saline, Group Galectin-3 and Group Galectin-3＋TD139. The memory ability（escape latency） and learning ability（number of crossing platforms） were detected in Morris water maze test and space exploration experiment. The β-amyloid precursor protein in mice brain tissue was detected by immunofluorescence assay. Results The memory ability and learning ability in Group Galectin-3 were significantly reduced compared with those of the other two groups（P〈0.05）. The area of plaques of β-amyloid precursor protein in Group Galectin-3 was significantly greater than that of the other two groups（P〈0.01）. However, there was no statistical difference between Group Normal Saline and Group Galectin-3＋TD139（P〉0.05）. Conclusion Galectin-3 plays an important role in the occurrence and pathology progress of Alzheimer’s disease in mice. Galectin-3 can lead to reduced memory ability and learning ability in mice, just like the Alzheimer’s disease. Galectin-3 can promote the production of the plaques of β-amyloid precursor protein, and delay the progression of the disease through the antagonistic inhibitor TD139.

关 键 词： 阿尔茨海默病 淀粉样前体蛋白

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