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Biomol Ther (Seoul). 2017 May 1;25(3):249-258. doi: 10.4062/biomolther.2016.058.

Biflorin Ameliorates Memory Impairments Induced by Cholinergic Blockade in Mice.

Jeon SJ1,2, Kim B1,2, Ryu B1,2, Kim E1,2, Lee S1,2, Jang DS1,2, Ryu JH1,2.

Author information

1
Department of Life and Nanopharmaceutical Science, College of Pharmacy, Kyung Hee University, Seoul 02447, Republic of Korea.
2
Kyung Hee East-West Pharmaceutical Research Institute, College of Pharmacy, Kyung Hee University, Seoul 02447, Republic of Korea.

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.

KEYWORDS:

Biflorin; Cognition; N-methyl D-aspartate receptor; Protein kinase C-ζ

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