A study on mechanism of tryptophan metabolic key enzymes protecting the brain environment by food ingredients

2016 Fiscal Year Final Research Report

• Project/Area Number: 26450150
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Food science
• Research Institution: Chiba University
• Principal Investigator: Egashira Yukari 千葉大学, 大学院園芸学研究科, 教授 (80213528)
• Research Collaborator: KOSHIGUCHI Manami ; HIRAI Shizuka
• Project Period (FY): 2014-04-01 – 2017-03-31
• Keywords: トリプトファン / NAD / ナイアシン / キノリン酸 / ファイトケミカル / 炎症 / ミクログリア / ACMSD

Outline of Final Research Achievements

Enhanced indoleamine 2, 3-dioxygenase (IDO) or decreased amino carboxymuconate semialdehyde decarboxylase (ACMSD) expression leads to increased levels of toxic metabolite quinolinic acid. In this study, we investigated the regulatory mechanism of tryptophan metabolic key enzymes by food ingredients. We found energy restricted diet increased ACMSD activity, and rat ACMSD was regulated by the transcription factor HNF4 alpha and other transcription factors.
Moreover, we examined the effect of ferulic acid (FA) in microglial cells on IDO expression levels and its mechanism. FA suppressed LPS-induced IDO mRNA expression and also suppressed nuclear translocation of NF-κB and phosphorylation of p38 MAPK in microglial cells. Our results indicate that FA decreases LPS-induced IDO expression, which may be mediated by suppression of the NF-κB and p38 MAPK pathways.

Free Research Field

食品科学