Effects of safflower yellow on beta-amyloid deposition and activation of astrocytes in the brain of APP/PS1 transgenic mice
Effects of safflower yellow on beta-amyloid deposition and activation of astrocytes in the brain of APP/PS1 transgenic mice
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红花黄色素对APP/PS1转基因小鼠脑内β-淀粉样蛋白沉积和星形胶质细胞活化的影响
DOI：
10.1016/j.biopha.2017.12.099
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发表时间：
2018
影响因子：
7.5
通讯作者：
Hu Yan li
中科院分区：
文献类型：
--
作者：
Shi Xiao meng;Zhang Hua;Zhou Zhang jiuzhi;Ruan Ying ying;Pang Jie;Zhang Lu;Zhai Wei;Hu Yan li
红花黄(SY)是从红花中提取的一种中药，通过抑制氧化损伤、神经元凋亡和tau蛋白过度磷酸化，对血管性痴呆和阿尔茨海默病(AD)动物模型具有神经保护作用。本研究旨在探讨红花黄(SY)能否改善AD模型小鼠的认知功能，减少淀粉样蛋白(Aβ，Aβ)积聚，减少星形胶质细胞过度激活。我们发现，SY治疗显著改善了APP/PS1小鼠的学习和记忆障碍。苏木精-伊红染色发现，SY治疗可减少APP/PS1小鼠神经元的丢失和死亡。免疫组织化学染色显示，SY显著下调APP/β小鼠A GFAP1-42沉积和胶质纤维酸性蛋白水平。生化分析还显示，SY处理降低了APP/PS1小鼠大脑皮质中可溶性和不溶性Aβ1-42的水平，以及海马区的可溶性Aβ1-42的水平。此外，我们发现SY处理降低了与Aβ生成相关的蛋白的表达，并显著增加了与Aβ清除相关的酶在APP/PS1小鼠脑组织中的表达。这些结果表明，SY可作为治疗AD的一种有前途的治疗方法。
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 Aβ1-42deposition and glial fibrillary acidic protein (GFAP) level in APP/PS1 mice. Biochemical analysis also showed that SY treatment reduced soluble and insoluble Aβ1-42level in the cortex and soluble Aβ1-42level 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.