| 陈志滨,曾玲,文红梅,李勇.姜黄素上调GRIA1调节突触可塑性拮抗帕金森病认知障碍.[J].中南医学科学杂志.,2024,(4):544-548. |
| 姜黄素上调GRIA1调节突触可塑性拮抗帕金森病认知障碍 |
| Curcumin regulates synaptic plasticity upregulating GRIA1 to counteract cognitive impairment in Parkinson's disease |
| 投稿时间：2024-01-16 修订日期：2024-05-15 |
| DOI：10.15972/j.cnki.43-1509/r.2024.04.009 |
| 中文关键词: 帕金森病认知障碍 姜黄素 GRIA1 突触可塑性 |
| 英文关键词:Parkinson's disease cognitive impairment curcumin GRIA1 synaptic plasticity |
| 基金项目:湖南省卫生健康委科研计划项目(202103072287) |
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| 中文摘要: |
| 目的探讨姜黄素通过上调GRIA1调节突触可塑性对帕金森病(PD)认知障碍的影响。 方法选取4只大鼠为对照组；20只大鼠单侧脑纹状体内注射6-OHDA构建PD认知功能障碍大鼠模型,随机均分为PD组、PD+Cur组、PD+LY341495组和PD+Cur+LY341495组。采用Y迷宫和Morris水迷宫测试大鼠的学习记忆能力,免疫荧光染色观察脑纹状体突触后致密物(PSD95)及AMPA受体(GluR2)的数量,Western blotting和qRT-PCR检测大鼠脑纹状体谷氨酸离子型受体AMPA型亚单位1(GRIA1)的蛋白及mRNA表达。 结果与对照组比较,PD组正确替换率、PSD95、GluR2表达减少,逃逸潜伏期延长,通过平台次数、目标象限停留时间、GRIA1蛋白及mRNA表达减少,路易小体数量增加(P＜0.05)。与PD组比较,PD+Cur组正确替换速率、PSD95、GluR2表达上升,逃逸潜伏期降低,通过平台次数、目标象限停留时间、GRIA1蛋白及mRNA表达增加,路易小体数量减少；而PD+LY341495组和PD+Cur+LY341495组变化趋势与PD+Cur组相反(P＜0.05)。 结论姜黄素可拮抗PD认知障碍,其机制可能是通过上调GRIA1调节突触可塑性实现的。 |
| 英文摘要: |
| AimTo explore the effect of curcumin on cognitive impairment in Parkinson's disease (PD) by upregulating GRIA1 to regulate synaptic plasticity. Methods4 rats were selected as control group. 20 rats were established a rat model of Parkinson's disease (PD) with cognitive impairment by unilaterally injecting 6-OHDA into the striatum, and the mice were randomly divided into PD group, PD+Cur group, PD+LY341495 group and PD+Cur+LY341495 group. The learning and memory abilities of the rats were assessed by using the Y-maze and Morris water maze tests. Immunofluorescence staining was performed to observe the quantity of postsynaptic density protein 95 (PSD95) and AMPA receptors (GluR2) in the striatum. Western blotting and qRT-PCR were conducted to measure the expression of glutamate ionotropic receptor AMPA type subunit 1 (GRIA1) protein and mRNA. ResultsCompared with the control group, the PD group showed a decrease in correct replacement rate, expression of PSD95 and GluR2, prolonged escape latency, decreased number of passes through the platform, target quadrant residence time, GRIA1 protein and mRNA expression, and an increase in the number of Lewy bodies (P＜0.05). Compared with the PD group, the PD+Cur group showed an increase in correct replacement rate, expression of PSD95 and GluR2, a decrease in escape latency, an increase in platform frequency, target quadrant residence time, GRIA1 protein and mRNA expression, and a decrease in the number of Lewy bodies. The trend of changes in the PD+LY341495 group and the PD+Cur+LY341495 group was opposite to that in the PD+Cur group (P＜0.05). ConclusionCurcumin can counteract cognitive impairment in Parkinson's disease (PD), and its mechanism may involve the modulation of synaptic plasticity through the upregulation of GRIA1. |
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