糖尿病脑病是糖尿病严重并发症之一，病变机制不明，目前缺乏有效的治疗药物。研究表明，神经细胞凋亡与糖尿病脑病发生关系密切。本项目组通过前期研究和研究文献，提出糖尿病脑病发生的一个可能机制，转录因子Sp1调控mylk1基因组蛋白乙酰化水平，引起基因mylk1（编码MLCK的基因）表达增高，高表达的MLCK促使海马神经元凋亡增加，导致认知功能障碍。制何首乌通过影响Sp1转录因子、基因mylk1组蛋白乙酰化水平、mylk1表达水平，抑制海马神经元凋亡，最终改善认知功能障碍。据此，本项目拟在细胞和动物两个水平，探讨Sp1通过调控mylk1组蛋白乙酰化水平引起神经细胞凋亡，导致认知功能障碍的作用机制，及制何首乌通过该机制抑制神经细胞凋亡，改善糖尿病认知功能障碍大鼠的认知功能。本项目研究将有助于阐明糖尿病脑病的发病机制，为糖尿病脑病的诊断和防治提供有价值的信息，为制何首乌的临床应用提供理论和实验依据。

Diabetic encephalopathy is one of the serious complications of diabetes, the pathogenesis of the disease is unclear and there is no effective treatment at present. Studies have shown that nerve cells apoptosis is closely related with the occurrence of diabetic encephalopathy. We proposed a possible mechanism of the occurrence of diabetic encephalopathy through our previous study and research papers. The transcription factor Sp1 regulates mylk1 histone acetylation level, resulted the expression of mylk1 (encoding MLCK )upgrading, and the upgraded expression of MLCK promotes hippocampal neurons apoptosis increasing, then increased apoptotic cells leads to cognitive dysfunction. Radix Polygoni Multiori inhibits hippocampal neuronal apoptosis and ultimately improves cognitive dysfunction by affecting transcription factor Sp1, mylk1 histone acetylation level, and mylk1 expression level.Accordingly, we speculate the mechanism of Sp1 inducing nerve cell apoptosis by regulating the level of mylk1 histone acetylation, and ultimately leading to cognitive dysfunction in cell and animal levels.Radix Polygoni Multiori inhibits nerve cells apoptosis and improves cognitive function of the diabetic rats. The study will help to clarify the of diabetic encephalopathy, provide valuable information for the diagnosis and prevention of diabetic encephalopathy, and provide theoretical and experimental basis for the clinical application of Radix Polygoni Multiori.