Biomol Ther (Seoul)  
Biflorin Ameliorates Memory Impairments Induced by Cholinergic Blockade in Mice
Se Jin Jeon1,2,†, Boseong Kim1,2,†, Byeol Ryu1,2, Eunji Kim1,2, Sunhee Lee1,2, Dae Sik Jang1,2,* and Jong Hoon Ryu1,2,*
1Department of Life and Nanopharmaceutical Science, 2Kyung Hee East-West Pharmaceutical Research Institute, College of Pharmacy, Kyung Hee University, Seoul 02447, Republic of Korea
E-mail: jhryu63@khu.ac.kr (Ryu JH), dsjang@khu.ac.kr (Jang DS)
Tel: +82-2-961-9230 (Ryu JH), +82-2-961-0719 (Jang DS)
Fax: +82-2-966-3885 (Ryu JH), +82-2-966-3885 (Jang DS)
The first two authors contributed equally to this work.
Received: March 15, 2016; Revised: June 9, 2016; Accepted: July 28, 2016; Published online: November 8, 2016.
© The Korean Society of Applied Pharmacology. All rights reserved.

Abstract
To examine the effect of biflorin, a component of Syzygium aromaticum, on memory deficit, we introduced a scopolamine-induced cognitive deficit mouse model. A single administration of biflorin increased latency time in the passive avoidance task, ameliorated alternation behavior in the Y-maze, and increased exploration time in the Morris water maze task, indicating the improvement of cognitive behaviors against cholinergic dysfunction. The biflorin-induced reverse of latency in the scopolamine-treated group was attenuated by MK-801, an NMDA receptor antagonist. Biflorin also enhanced cognitive function in a na?ve mouse model. To understand the mechanism of biflorin for memory amelioration, we performed Western blot. Biflorin increased the activation of protein kinase C-ζ and its downstream signaling molecules in the hippocampus. These results suggest that biflorin ameliorates drug-induced memory impairment by modulation of protein kinase C-ζ signaling in mice, implying that biflorin could function as a possible therapeutic agent for the treatment of cognitive problems.
Keywords: Biflorin, N-methyl D-aspartate receptor, Cognition, Protein kinase C-ζ


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