论文部分内容阅读
目的考察梓醇对血管性痴呆(VD)大鼠学习记忆能力及海马Bax、Bcl-2蛋白表达的影响。方法采用双侧颈总动脉结扎来制备VD大鼠模型,造模后第30天,将大鼠分成模型组、阳性组及梓醇高、中、低剂量组,连续给药30 d。采用Morris水迷宫法检测大鼠的学习记忆能力,HE染色法观察海马CA1区的病理组织形态,免疫组化法检测海马CA1区Bax和Bcl-2蛋白的表达。结果与模型组相比,高、中剂量组大鼠第3、4天的逃避潜伏期明显缩短,高、中、低剂量梓醇组大鼠的站台穿越次数明显增加;梓醇能改善大鼠海马CA1区神经元的病理改变;梓醇高、中剂量能下调促凋亡蛋白Bax的表达,上调抑凋亡蛋白Bcl-2的表达。结论梓醇能改善VD大鼠的学习记忆能力,其机制可能与抑制海马神经细胞凋亡有关。
Objective To investigate the effects of catalpol on the learning and memory ability and the expression of Bax and Bcl-2 in hippocampus of vascular dementia (VD) rats. Methods The bilateral common carotid arteries were ligated to prepare VD model rats. On the 30th day after model establishment, the rats were divided into model group, positive group and catalpol high, medium and low dose groups for continuous administration for 30 days. Morris water maze test was used to detect the learning and memory abilities of rats. HE staining was used to observe the histopathology of hippocampal CA1 region. The expression of Bax and Bcl-2 protein in hippocampal CA1 region was detected by immunohistochemistry. Results Compared with the model group, the escape latency of rats in the high and middle dose groups was significantly shortened at day 3 and 4, and the number of platform crossings in the high, medium and low dose catalpol groups increased significantly. Catalpol improved the hippocampus CA1 area neurons pathological changes; Catalpol high and medium dose can down-regulate the expression of pro-apoptotic protein Bax, up-regulate the expression of anti-apoptotic protein Bcl-2. Conclusion Catalpol can improve the learning and memory abilities of VD rats, and its mechanism may be related to inhibiting the apoptosis of hippocampal neurons.