Active Constituents from Drynaria fortunei Rhizomes on the Attenuation of Aβ25-35-Induced Axonal Atrophy

Zhi You Yang; Tomoharu Kuboyama; Kohei Kazuma; Katsuhiro Konno; Chihiro Tohda

doi:10.1021/acs.jnatprod.5b00290

Active Constituents from Drynaria fortunei Rhizomes on the Attenuation of Aβ_25-35-Induced Axonal Atrophy

Zhi You Yang, Tomoharu Kuboyama, Kohei Kazuma, Katsuhiro Konno, Chihiro Tohda^*

^*Corresponding author for this work

Section of Neuromedical Science, Division of Bioscience, Institute of Natural Medicine

Research output: Contribution to journal › Article › peer-review

36 Scopus citations

Abstract

Axonal regeneration might contribute to the restoration of damaged neuronal networks and improvement of memory deficits in a murine Alzheimers disease (AD) model. A search for axonal regenerative drugs was performed to discover novel therapeutic options for AD. In this study, an aqueous extract of Drynaria fortunei rhizomes reversed Aβ_25-35-induced axonal atrophy in cultured cortical neurons of mice. Bioassay-guided fractionation of this extract led to the isolation and identification of compounds 1-5. Among them, (2S)-neoeriocitrin (2) and caffeic acid 4-O-glucoside (4) showed significant axonal elongation effects on Aβ_25-35-induced atrophy.

Original language	English
Pages (from-to)	2297-2300
Number of pages	4
Journal	Journal of Natural Products
Volume	78
Issue number	9
DOIs	https://doi.org/10.1021/acs.jnatprod.5b00290
State	Published - 2015/09/25

ASJC Scopus subject areas

Analytical Chemistry
Molecular Medicine
Pharmacology
Pharmaceutical Science
Drug Discovery
Complementary and alternative medicine
Organic Chemistry

Access to Document

10.1021/acs.jnatprod.5b00290

Cite this

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title = "Active Constituents from Drynaria fortunei Rhizomes on the Attenuation of Aβ25-35-Induced Axonal Atrophy",

abstract = "Axonal regeneration might contribute to the restoration of damaged neuronal networks and improvement of memory deficits in a murine Alzheimers disease (AD) model. A search for axonal regenerative drugs was performed to discover novel therapeutic options for AD. In this study, an aqueous extract of Drynaria fortunei rhizomes reversed Aβ25-35-induced axonal atrophy in cultured cortical neurons of mice. Bioassay-guided fractionation of this extract led to the isolation and identification of compounds 1-5. Among them, (2S)-neoeriocitrin (2) and caffeic acid 4-O-glucoside (4) showed significant axonal elongation effects on Aβ25-35-induced atrophy.",

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AU - Konno, Katsuhiro

AU - Tohda, Chihiro

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AB - Axonal regeneration might contribute to the restoration of damaged neuronal networks and improvement of memory deficits in a murine Alzheimers disease (AD) model. A search for axonal regenerative drugs was performed to discover novel therapeutic options for AD. In this study, an aqueous extract of Drynaria fortunei rhizomes reversed Aβ25-35-induced axonal atrophy in cultured cortical neurons of mice. Bioassay-guided fractionation of this extract led to the isolation and identification of compounds 1-5. Among them, (2S)-neoeriocitrin (2) and caffeic acid 4-O-glucoside (4) showed significant axonal elongation effects on Aβ25-35-induced atrophy.

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