Biflorin Ameliorates Memory Impairments Induced by Cholinergic Blockade in Mice.
10.4062/biomolther.2016.058
- Author:
Se Jin JEON
1
;
Boseong KIM
;
Byeol RYU
;
Eunji KIM
;
Sunhee LEE
;
Dae Sik JANG
;
Jong Hoon RYU
Author Information
1. Department of Life and Nanopharmaceutical Science, Republic of Korea. jhryu63@khu.ac.kr
- Publication Type:Original Article
- Keywords:
Biflorin;
N-methyl D-aspartate receptor;
Cognition;
Protein kinase C-ζ
- MeSH:
Animals;
Blotting, Western;
Cognition;
Cognition Disorders;
Dizocilpine Maleate;
Hippocampus;
Memory Disorders;
Memory*;
Mice*;
N-Methylaspartate;
Protein Kinases;
Syzygium;
Water
- From:Biomolecules & Therapeutics
2017;25(3):249-258
- CountryRepublic of Korea
- Language:English
-
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 naïve 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.
