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目的:研究知母皂苷(SAa B)对Aβ1-42诱导的大鼠学习记忆障碍的改善作用及机制。方法:选用SD大鼠48只随机分为4组:正常对照组,Aβ1-42组,SAa B(1、2.5 mg/ml)+Aβ1-42组,每组12只,侧脑室注射给药后第2 d进行Morris水迷宫实验,第7d快速取海马CA1区,Western Blot法观察磷酸化tau(P-tau)、磷酸化GSK-3β、磷酸化Akt蛋白及胆碱乙酰基转移酶(Ch AT)蛋白表达水平。结果:脑室内注射Aβ1-42大鼠出现明显的空间学习记忆障碍,表现为逃避潜伏期和游泳路程较正常对照组明显延长,在原平台象限游泳时间占总时间的百分比明显降低,同时伴有海马P-tau表达明显增加,p-GSK-3β、p-Akt、Ch AT表达明显降低。侧脑室内注射SAa B后,与Aβ1-42组相比,SAa B(1、2.5 mg/ml)+Aβ1-42组大鼠逃避潜伏期和游泳路程明显缩短,原平台象限游泳时间占总游泳时间百分比升高;海马P-tau表达明显降低,p-GSK-3β、p-Akt、Ch AT表达明显增加。结论:侧脑室内注射知母皂苷可通过降低Ptau表达水平,提高Ch AT活性,从而减少神经元纤维缠结的形成,并可能通过调节胆碱能功能的途径发挥抗痴呆的作用。
Objective: To study the effects of saponin (SAa B) on Aβ1-42 induced learning and memory impairment in rats and its mechanism. Methods: Forty-eight SD rats were randomly divided into 4 groups: normal control group, Aβ1-42 group, SAa B (1,2.5 mg / ml) + Aβ1-42 group, 12 in each group. After intracerebroventricular injection Morris water maze test was performed on day 2, and the hippocampal CA1 region was rapidly detected on the 7th day. The phosphorylated tau (P-tau), phosphorylated GSK-3β, phospho-Akt and ChAT ) Protein expression level. Results: The spatial learning and memory impairment occurred in the intracerebroventricular injection of Aβ1-42, which showed that the escape latency and swimming distance were significantly longer than those in the normal control group. The swimming time in the original platform quadrant decreased significantly as a percentage of the total time, -tau expression was significantly increased, p-GSK-3β, p-Akt, Ch AT significantly decreased. Compared with Aβ1-42 group, SAa B (1,2.5 mg / ml) + Aβ1-42 group had significantly shorter escape latency and swimming distance compared with Aβ1-42 group, and the former platform quadrant swimming time accounted for the total swimming time The percentage of P-tau in hippocampus was significantly decreased, and the expression of p-GSK-3β, p-Akt, Ch AT was significantly increased. CONCLUSION: Intracerebroventricular injection of timosaponin can reduce the formation of neurofibrillary tangles by decreasing the expression of Ptau, increasing the activity of ChAT, and may play an anti-dementia effect through the regulation of cholinergic function.