D-半乳糖联合三氯化铝对C57小鼠海马Bcl2表达的影响

摘要

目的 探讨D-半乳糖联合三氯化铝(AlCl3)对C57小鼠海马B淋巴细胞瘤-2(Bcl2)表达的影响及在阿尔茨海默病(AD)发病中的意义.方法 D-半乳糖90 mg·kg-1·d-1联合AlCl3 40 mg·kg-1·d-1连续90 d腹腔注射制造AD小鼠模型;通过比较全脑图片及糖水实验初步鉴定模型复制是否成功;免疫组化检测AD及野生型对照组小鼠海马CA1、CA3和DG区Bcl2蛋白表达水平.结果 与对照组比较,AD小鼠完整脑组织表面泛白、无血色,血管明显减少.糖水偏好实验:与对照组比较,AD组小鼠糖水偏好百分比明显下降(P<0.01).与对照组相比,AD小鼠海马CA1、CA3和DG区Bcl2蛋白阳性表达明显减少,呈深棕色阳性颗粒数目明显减少(CA1、CA3区P<0.05;DG区P<0.01).结论 D-半乳糖联合AlCl3通过抑制Bcl2的表达,导致海马神经细胞异常凋亡,进而引起AD的发生、发展.%Objective To investigate the expression and significance of Bcl2 in Alzheimer's disease (AD) and wild type mice hippocampus.Methods D-galactose 90 mg·kg-1·d-1 and AlCl3 40 mg·kg-1·d-1 continuous intraperitoneal injection of 90 days to make AD mouse model;preliminary appraise AD model by comparing the whole brain images and object recognition experiment.Bcl2 protein expression level was compared in AD and wild type control mice hippocampal CA1, CA3 and DG areas by immunohistochemical detection.Results Compared with control group, AD mice brain tissue surface suffused with white color, significantly less blood vessels.The time of AD group used to explore new object was significant less than wild type control group (P<0.01);The discrimination index difference between AD model (10.07±1.33) and wild type control group (33.97±3.74) was very significant.Compared with the wild type control group, the positive expression of Bcl2 protein in hippocampal CA1, CA3 and DG areas were significantly decreased (P<0.05,P<0.01).Conclusions D-galactose combined with AlCl3 could inhibit the expression of Bcl2 resulting in abnormal apoptosis of hippocampal neurons, which could lead to the occurrence and development of AD.