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水飞蓟宾(CDRI-08)的一种特殊提取物恢复了氯化钴低氧模拟小鼠的记忆,这与海马体中Fmr-1基因表达上调有关。

A Special Extract of Bacopa monnieri (CDRI-08)-Restored Memory in CoCl2-Hypoxia Mimetic Mice Is Associated with Upregulation of Fmr-1 Gene Expression in Hippocampus.

作者信息

Rani Anupama, Prasad S

机构信息

Biochemistry & Molecular Biology Lab, Centre of Advanced Study in Zoology, Banaras Hindu University, Uttar Pradesh, Varanasi 221005, India.

出版信息

Evid Based Complement Alternat Med. 2015;2015:347978. doi: 10.1155/2015/347978. Epub 2015 Aug 27.

Abstract

Fragile X mental retardation protein (FMRP) is a neuronal translational repressor and has been implicated in learning, memory, and cognition. However, the role of Bacopa monnieri extract (CDRI-08) in enhancing cognitive abilities in hypoxia-induced memory impairment via Fmr-1 gene expression is not known. Here, we have studied effects of CDRI-08 on the expression of Fmr-1 gene in the hippocampus of well validated cobalt chloride (CoCl2)-induced hypoxia mimetic mice and analyzed the data with alterations in spatial memory. Results obtained from Morris water maze test suggest that CoCl2 treatment causes severe loss of spatial memory and CDRI-08 is capable of reversing it towards that in the normal control mice. Our semiquantitative RT-PCR, Western blot, and immunofluorescence microscopic data reveal that CoCl2-induced hypoxia significantly upregulates the expression of Hif-1α and downregulates the Fmr-1 expression in the hippocampus, respectively. Further, CDRI-08 administration reverses the memory loss and this is correlated with significant downregulation of Hif-1α and upregulation of Fmr-1 expression. Our data are novel and may provide mechanisms of hypoxia-induced impairments in the spatial memory and action of CDRI-08 in the recovery of hypoxia led memory impairment involving Fmr-1 gene encoded protein called FMRP.

摘要

脆性X智力低下蛋白(FMRP)是一种神经元翻译抑制因子,与学习、记忆和认知有关。然而,假马齿苋提取物(CDRI-08)通过Fmr-1基因表达增强缺氧诱导的记忆障碍中的认知能力的作用尚不清楚。在此,我们研究了CDRI-08对经过充分验证的氯化钴(CoCl2)诱导的缺氧模拟小鼠海马中Fmr-1基因表达的影响,并分析了空间记忆改变的数据。莫里斯水迷宫试验获得的结果表明,CoCl2处理会导致严重的空间记忆丧失,而CDRI-08能够将其逆转至正常对照小鼠的水平。我们的半定量RT-PCR、蛋白质印迹和免疫荧光显微镜数据显示,CoCl2诱导的缺氧分别显著上调海马中Hif-1α的表达并下调Fmr-1的表达。此外,给予CDRI-08可逆转记忆丧失,这与Hif-1α的显著下调和Fmr-1表达的上调相关。我们的数据是新颖的,可能提供缺氧诱导的空间记忆损伤的机制以及CDRI-08在涉及Fmr-1基因编码的名为FMRP的蛋白质的缺氧导致的记忆损伤恢复中的作用机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/627b/4564622/7f23ba7133c2/ECAM2015-347978.001.jpg

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