A search for anti-inflammatory mechanisms via AMPK activation by an oral nucleotide related umami compound.

2020 Fiscal Year Final Research Report

• Project/Area Number: 17K19941
• Research Category: Grant-in-Aid for Challenging Research (Exploratory)
• Allocation Type: Multi-year Fund
• Research Field: Health science and related fields
• Research Institution: Beppu University
• Principal Investigator: Kimura Yasuhiro 別府大学, 食物栄養科学部, 教授 (90549792)
• Project Period (FY): 2017-06-30 – 2021-03-31
• Keywords: 核酸系旨味物質 / AMP / AMPK / 炎症性大腸疾患 / 抗炎症作用

Outline of Final Research Achievements

We tested the proportions of Th1, Th17, and Treg cells in the lamina propria of the colon in DSS-induced IBD mice fed the diet with AMP using a flow cytometry in understanding mechanisms of the anti-inflammatory effects via AMPK activation by an oral adenosine-5’-monophosphate (AMP) administration.
The mice fed the diet with AMP had greater improvement of severity of the colitis as watery and bloody diarrhea. The flow cytometry analysis indicated that AMP administration had lower tendencies in proportions of pro-inflammatory Th1 and anti-inflammatory Treg cells in the lamina propria as compared to those of IBD mice fed the diet without AMP, but not significantly different. The results of the immunohistochemistry analysis showed that AMP was likely to elicit mild infiltration of Treg cells to the colon tissues compared to those in IBD mice fed the diet without AMP. Take together, AMP may have an effect for attenuating infiltration of T helper cells into inflamed tissues of the colon.

Free Research Field

食品機能学、栄養・腸管生理学

Academic Significance and Societal Importance of the Research Achievements

潰瘍性大腸炎やクローン病に代表される炎症性腸疾患（IBD）は、寛解と再燃を繰り返す難治性疾患で、未だ発症原因も不明であり、治療の中心は薬物による対症療法で、決定的な根治療法は確立されていない。研究者は動物実験ではあるが、核酸系旨味物質のAMPによるAMPKの活性化を介してIBDの病状が抑えられることを発見している。本研究では、AMPの投与により炎症をコントロールする免疫細胞の大腸組織への浸潤が抑制される可能性を示唆するデータを得ることができた。今後、核酸系旨味物質をIBD治療へ応用することを目標にさらに作用メカニズムの探索を進め将来的に臨床応用につなげたい。