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目的:探讨齐墩果酸唤醒阿尔兹海默病(AD)大鼠沉默突触而改善其认知功能的作用及初步机制。方法:选用雄性SD大鼠,经侧脑室注射Aβ25-35建立AD模型,通过水迷宫实验检测大鼠空间学习与记忆能力,采用透视电镜观察神经元及突触超微结构,Western blot检测钙调蛋白激酶Ⅱ(Ca MKⅡ)、蛋白激酶C(PKC)、脑源性神经营养因子(BDNF)以及酪氨酸激酶受体B(Trk B)蛋白表达。结果:与正常组比较,模型组大鼠的逃避潜伏时间明显延长(P<0.01),空间学习与记忆能力明显下降,神经元与突触超微结构损伤明显,Ca MKⅡ、PKC、BDNF及Trk B蛋白表达明显减少(P<0.01);与模型组比较,齐墩果酸组大鼠的逃避潜伏时间明显缩短(P<0.01),学习与记忆能力显著提高,神经元与突触超微结构损伤减轻,Ca MKⅡ、PKC、BDNF及Trk B蛋白表达明显增加(P<0.01)。结论:齐墩果酸可有效改善AD大鼠的空间学习与记忆能力,该作用可能与减轻神经元及突触超微结构损伤和唤醒沉默突触有关。
Objective: To investigate the effect and primary mechanism of oleanolic acid in ameliorating cognitive function by silencing synapse in Alzheimer’s disease (AD) rats. Methods: Male Sprague-Dawley rats were used to establish AD model by injection of Aβ25-35 into the lateral ventricle. The spatial learning and memory ability of the rats was examined by water maze test. The ultrastructure of neurons and synapses were observed by electron microscopy. Protein kinase C (PKC), brain derived neurotrophic factor (BDNF) and tyrosine kinase receptor B (Trk B) protein expression. Results: Compared with the normal group, the escape latency of the model group was significantly longer (P <0.01), the learning and memory abilities of the model group were significantly decreased, the damage of neurons and synaptic ultrastructure were obvious, and the expressions of Ca MKⅡ, PKC, BDNF and Trk (P <0.01). Compared with the model group, the escape latency of the oleanolic acid group was significantly shortened (P <0.01), and the learning and memory ability was significantly increased. Compared with the model group, the neuronal and synaptic ultrastructure Injury alleviated, and expressions of Ca MKⅡ, PKC, BDNF and Trk B were significantly increased (P <0.01). Conclusion: Oleanolic acid can effectively improve spatial learning and memory in AD rats, which may be related to the reduction of neuronal and synaptic ultrastructure damage and the awakening of silent synapses.