Key Laboratory of Xinjiang Phytomedicine Resource and Utilization, Ministry of Education, Department of Pharmacology, Shihezi University, Shihezi, Xinjiang 832000, PR China; Psychosis Welfare Institution, Urumchi, Xinjiang 830023, PR China.
Key Laboratory of Xinjiang Phytomedicine Resource and Utilization, Ministry of Education, Department of Pharmacology, Shihezi University, Shihezi, Xinjiang 832000, PR China.
Biomed Pharmacother. 2018 Feb;98:553-565. doi: 10.1016/j.biopha.2017.12.099. Epub 2017 Dec 27.
Safflower yellow (SY), one of traditional Chinese medicine extracted from safflower, has been shown to have neuroprotective effects on animal models of vascular dementia and Alzheimer's diseases (AD), by inhibiting oxidative injury, neuronal apoptosis and tau hyperphosphorylation. In this study, we investigated whether safflower yellow (SY) can improve cognitive function, decrease Amyloid β (Aβ) accumulation and overactivation of astrocytes in AD mouse model. We found that SY treatment significantly ameliorated the learning and memory deficits of APP/PS1 mice. By hematoxylin-eosin staining, we found that the neuronal loss and death in APP/PS1 mice was decreased by SY treatment. Immunohistochemical staining showed that SY treatment dramatically down-regulated Aβ deposition and glial fibrillary acidic protein (GFAP) level in APP/PS1 mice. Biochemical analysis also showed that SY treatment reduced soluble and insoluble Aβ level in the cortex and soluble Aβ level in the hippocampus of APP/PS1 mice. Moreover, we found that SY treatment decreased the expression of proteins related to generation of Aβ, and markedly increased expression of enzymes associated with clearance of Aβ in the brain of APP/PS1 mice. These results indicate that the SY can serve as a promising therapeutic approach for the treatment of AD.
红花黄色素（SY）是一种从红花中提取的中药，已被证明对血管性痴呆和阿尔茨海默病（AD）的动物模型具有神经保护作用，可抑制氧化损伤、神经元凋亡和tau 过度磷酸化。在本研究中，我们研究了红花黄色素（SY）是否可以改善 AD 小鼠模型的认知功能，减少淀粉样蛋白β（Aβ）积累和星形胶质细胞过度激活。我们发现 SY 治疗可显著改善 APP/PS1 小鼠的学习和记忆缺陷。通过苏木精-伊红染色，我们发现 SY 治疗可减少 APP/PS1 小鼠的神经元丢失和死亡。免疫组织化学染色显示，SY 治疗可显著下调 APP/PS1 小鼠的 Aβ 沉积和神经胶质纤维酸性蛋白（GFAP）水平。生化分析还表明，SY 治疗可降低 APP/PS1 小鼠大脑皮质中的可溶性和不溶性 Aβ 水平以及海马中的可溶性 Aβ 水平。此外，我们发现 SY 治疗可降低与 Aβ 生成相关的蛋白表达，并显著增加 APP/PS1 小鼠大脑中与 Aβ 清除相关的酶的表达。这些结果表明，SY 可作为治疗 AD 的一种有前途的治疗方法。
