（-）-SCR1693 可预防慢性脑低灌注大鼠模型的记忆障碍和海马损伤。
(-)-SCR1693 Protects against Memory Impairment and Hippocampal Damage in a Chronic Cerebral Hypoperfusion Rat Model.
机构信息
Department of Pharmacology, Shandong Univeristy School of Medicine 44#, Wenhua Xi Road, Jinan, Shandong, 250012 P.R. China.
School of Pharmacy, Key Laboratory of Molecular Pharmacology and Drug Evaluation (Yantai University), Ministry of Education, Collaborative Innovation Center of Advanced Drug Delivery System and Biotech Drugs in Universities of Shandong, Yantai University, Yantai 264005, P.R. China.
出版信息
Sci Rep. 2016 Jun 28;6:28908. doi: 10.1038/srep28908.
Chronic cerebral hypoperfusion (CCH) is one of the most common causes of vascular dementia (VaD) and is recognised as an etiological factor in the development of Alzheimer's disease (AD). CCH can induce severe cognitive deficits, as assessed by the water maze task, along with neuronal loss in the hippocampus. However, there are currently no effective, approved pharmacological treatments available for VaD. In the present study, we created a rat model of CCH using bilateral common carotid artery occlusion and found that (-)-SCR1693, a novel compound, prevented rats from developing memory deficits and neuronal damage in the hippocampus by rectifying cholinergic dysfunction and decreasing the accumulation of the phospho-tau protein. These results strongly suggest that (-)-SCR1693 has therapeutic potential for the treatment of CCH-induced VaD.
慢性脑灌注不足（CCH）是血管性痴呆（VaD）最常见的原因之一，被认为是阿尔茨海默病（AD）发展的一个病因。CCH 可导致严重的认知缺陷，如在水迷宫任务中评估的那样，同时伴有海马神经元丢失。然而，目前尚无有效的、已批准的用于 VaD 的药物治疗方法。在本研究中，我们使用双侧颈总动脉闭塞建立了 CCH 大鼠模型，发现新型化合物 (-)-SCR1693 通过纠正胆碱能功能障碍和减少磷酸化 tau 蛋白的积累，防止大鼠出现记忆缺陷和海马神经元损伤。这些结果强烈表明，(-)-SCR1693 具有治疗 CCH 诱导的 VaD 的潜力。
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