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2017 Fiscal Year Final Research Report

Research for anti-inflammatory therapeutic strategy against pulmonary fibrosis

Research Project

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Project/Area Number 15K09546
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Collagenous pathology/Allergology
Research InstitutionGunma University

Principal Investigator

HISADA Takeshi  群馬大学, 医学部附属病院, 講師 (10344938)

Co-Investigator(Renkei-kenkyūsha) OKAJIMA Fumikazu  青森大学, 薬学部, 教授 (30142748)
Research Collaborator YATOMI Masakiyo  群馬大学, 医学部附属病院, 助教 (60784105)
SAITO Haruka  群馬大学, 医学部附属病院, 医員 (80447268)
Project Period (FY) 2015-04-01 – 2018-03-31
Keywords肺線維症 / 脂質メディエーター / resolvin / 炎症収束 / 動物モデル / ω-3脂肪酸
Outline of Final Research Achievements

Pulmonary fibrosis is a destructive inflammatory disease with limited therapeutic options. Resolvin D1 (RvD1) displays potent anti-inflammatory, pro-resolving activity. We tested the hypothesis that 17(R)-RvD1 can provide a therapeutic benefit by reducing inflammation and pulmonary fibrosis. Mice were exposed to bleomycin (BLM) to induce pulmonary fibrosis, and were then treated with 17(R)-RvD1. Administration of 17(R)-RvD1 from the start of BLM treatment attenuated neutrophil alveolar infiltration, lung collagen content, and IL-1β, TGF-β1, CTGF, and type I collagen mRNA expression, along with subsequent reduction in histologically detectable fibrosis. The administration of 17(R)-RvD1 at the later fibrotic stage also improved the lung failure. These results suggest that 17(R)-RvD1 attenuates pulmonary fibrosis by promoting the resolution of neutrophilic inflammation and also provides pulmonary restoration. These data highlight the therapeutic potential of 17(R)-RvD1.

Free Research Field

アレルギー・膠原病

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Published: 2019-03-29  

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