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2017 Fiscal Year Final Research Report

Elucidation of a destruction mechanism and development of new treatment on intraocular chronic inflammatory diseases with CYP metabolites

Research Project

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Project/Area Number 15K10869
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Ophthalmology
Research InstitutionYamaguchi University

Principal Investigator

YANAI Ryoji  山口大学, 医学部附属病院, 講師 (10346554)

Co-Investigator(Kenkyū-buntansha) 園田 康平  九州大学, 医学研究院, 教授 (10294943)
佐古田 幸美  山口大学, 大学院医学系研究科, 講師 (30629754)
折田 朋子  山口大学, 医学部附属病院, 助教 (50467792)
木村 和博  山口大学, 大学院医学系研究科, 教授 (60335255)
寺西 慎一郎  山口大学, 医学部附属病院, 助教 (90649360)
Project Period (FY) 2015-04-01 – 2018-03-31
Keywords眼炎症 / 加齢黄斑変性症 / ぶどう膜炎 / オメガ3脂肪酸 / チトクロームP
Outline of Final Research Achievements

We demonstrate that dietary supplementation of ω-3 LCPUFAs mediate choroidal neovessel regression with leukocyte recruitment and inflammatory reduction in choroidal neovascular lesions. Furthermore, we show that a diet enriched in ω-3 LCPUFAs suppressed uveitis in mice in association with inhibition of Th1 and Th17 cell function. cytochrome P450 (CYP) epoxygenases target the ω-3 double bond, resulting in an accumulation of 17,18-epoxyeicosatetraenoic acid (17,18-EEQ) derived from EPA, one of major ω-3 LCPUFAs.
In current study, we examined the anti-inflammatory properties of these molecules and have shown that 17,18-EEQ suppressed intraocular inflammation, as evaluated both clinically and histologically, in mice with EAU by inhibiting both systemic and retinal Th1 and Th17 cells.

Free Research Field

眼科学

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Published: 2019-03-29  

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