Safflower yellow attenuates learning and memory deficits in amyloid -induced Alzheimer's disease rats by inhibiting neuroglia cell activation and inflammatory signaling pathways
Safflower yellow attenuates learning and memory deficits in amyloid -induced Alzheimer's disease rats by inhibiting neuroglia cell activation and inflammatory signaling pathways
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红花黄通过抑制神经胶质细胞活化和炎症信号通路减轻淀粉样蛋白诱导的阿尔茨海默病大鼠的学习和记忆缺陷
DOI：
10.1007/s11011-019-00398-0
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发表时间：
2019-06-01
影响因子：
3.6
通讯作者：
Hu，Yanli
中科院分区：
文献类型：
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作者：
Zhang，Lu;Zhou，Zhangjiuzhi;Hu，Yanli
红花黄色素（SY）是天然红花的水提物。我们的实验室已经报道了SY在阿尔茨海默病转基因小鼠模型中减轻记忆障碍的保护作用。SY对痴呆中淀粉样蛋白-β诱导的神经炎症的可能有益作用仍不清楚。本研究假设星形胶质细胞和小胶质细胞可能引起淀粉样β蛋白沉积并产生神经炎症反应，旨在阐明SY在Aβ1- 42诱导的大鼠模型中调节胶质细胞活化和减少Aβ沉积的作用及其机制。Wistar大鼠在双侧海马注射聚集的Aβ1-42后给予SY治疗1个月;进行行为学测试以证明认知功能的改善。检测AD大鼠脑组织中iNOS、IL-1β、IL-6、TNF-α的含量。Western blot和实时荧光定量PCR检测M1和M2相关标志物，以证明小胶质细胞的活化。实验结果表明，SY能增强痴呆大鼠的空间学习记忆能力，降低iNOS、IL-1β、IL-6和TNF-α的含量，抑制胶质细胞的活化。此外，SY治疗抑制M1释放的促炎细胞因子（iNOS和CD 86），增加的表达，CD 206，YM-1，从而减少模型大鼠的炎症。提示SY对中药治疗AD的研究和开发具有重要的理论和临床价值。
Safflower yellow (SY) is an aqueous extract of natural safflower. Our laboratory has reported protective effects of alleviating memory impairment with SY in a transgentic mouse model of Alzheimer’s disease. The possible beneficial effects of SY on amyloid-β-induced neuroinflammation in dementia remain unclarified. This study we hypothesize that astrocytes and microglia may cause amyloid-β deposition and produce a neuroinflammatory response, aims to explain the role and mechanism of SY in regulating glial activation and reducing Aβ deposition in Aβ1–42induced rat model. Wistar rats were treated with SY for one month after bilateral hippocampal injection of aggregated Aβ1–42; behavioral tests were performed to demonstrate the amelioration of cognitive function. After that, the contents of iNOS, IL-1β, IL-6, and TNF-α in AD brain was detected. Western blot and real-time PCR were used to detect the M1 and M2-associated markers to demonstrate the activation of microglia. The conducted experiments have revealed that SY could strengthen spatial learning and memory ability of dementia rats, decrease the contents of iNOS, IL-1β, IL-6, and TNF-α and depress the activation of glial cells. Moreover, the SY treatment inhibited the M1 release of pro-inflammatory cytokines (iNOS and CD86), increased the expression of arginase-1, CD206, and YM-1 thereby reduced inflammation in model rats. Thus our results indicated that SY has very important theoretical and clinical value for the research and development of Chinese medicine for the treatment of AD.