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CJLJ103 通过增加 BDNF 表达和抑制 NF-κB 激活来减轻东莨菪碱诱导的小鼠记忆障碍。

CJLJ103 Attenuates Scopolamine-Induced Memory Impairment in Mice by Increasing BDNF Expression and Inhibiting NF-κB Activation.

机构信息

Neutrobiota Research Center, Kyung Hee University, Seoul 02447, Republic of Korea.

Department of Life and Nanopharmaceutical Sciences, College of Pharmacy, Kyung Hee University, Seoul 02447, Republic of Korea.

出版信息

J Microbiol Biotechnol. 2018 Sep 28;28(9):1443-1446. doi: 10.4014/jmb.1805.05025.

DOI:10.4014/jmb.1805.05025
PMID:30111074
Abstract

In the present study, we examined whether CJLJ103 (LJ) could alleviate cholinergic memory impairment in mice. Oral administration of LJ alleviated scopolamine-induced memory impairment in passive avoidance and Y-maze tasks. Furthermore, LJ treatment increased scopolamine-suppressed BDNF expression and CREB phosphorylation in the hippocampi of the brain, as well as suppressed TNF-α expression and NF-κB activation. LJ also increased BDNF expression in corticosterone-stimulated SH-SY5Y cells and inhibited NF-κB activation in LPS-stimulated microglial BV2 cells. However, LJ did not inhibit acetylcholinesterase activity. These findings suggest that LJ, a member of human gut microbiota, may mitigate cholinergic memory impairment by increasing BDNF expression and inhibiting NF-κB activation.

摘要

在本研究中,我们考察了 CJLJ103(LJ)是否可以缓解小鼠的胆碱能记忆损伤。LJ 的口服给药缓解了东莨菪碱诱导的被动回避和 Y 迷宫任务中的记忆损伤。此外,LJ 处理增加了脑内海马区受东莨菪碱抑制的 BDNF 表达和 CREB 磷酸化,并抑制了 TNF-α 表达和 NF-κB 激活。LJ 还增加了皮质酮刺激的 SH-SY5Y 细胞中的 BDNF 表达,并抑制了 LPS 刺激的小胶质细胞 BV2 细胞中的 NF-κB 激活。然而,LJ 并没有抑制乙酰胆碱酯酶的活性。这些发现表明,LJ,作为人类肠道微生物群的一员,可能通过增加 BDNF 表达和抑制 NF-κB 激活来减轻胆碱能记忆损伤。

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