Alteration of oxidative-stress and related marker levels in mouse colonic tissues and fecal microbiota structures with chronic ethanol administration

2021 Fiscal Year Final Research Report

• Project/Area Number: 18K11087
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Review Section: Basic Section 59040:Nutrition science and health science-related
• Research Institution: Kobe Gakuin University
• Principal Investigator: Ohira Hideo 神戸学院大学, 栄養学部, 准教授 (40351762)
• Co-Investigator(Kenkyū-buntansha): 中山 亨 東北大学, 工学研究科, 教授 (80268523)
• Project Period (FY): 2018-04-01 – 2022-03-31
• Keywords: アルコール / 飲酒習慣 / 腸内細菌 / 酸化ストレス / 大腸がん

Outline of Final Research Achievements

Chronic oral administration of ethanol in mice resulted in the elevation of colonic levels of oxidative stress markers, and this was consistently accompanied by elevated levels of inflammation-associated markers and a decreased level of regulatory T (Treg) cells. It also resulted in an alteration of mouse fecal microbiota structures, reminiscent of the alterations observed in human inflammatory bowel disease, and this appeared to be consistent with the proposed sustained generation of oxidative stress in the colonic environment during chronic ethanol consumption. Chronic ethanol administration results in elevated levels of advance glycation end products and their receptors (RAGE) in the colonic tissues in mice is also shown. Thus, enhancement of this pathway likely exacerbates the ethanol-induced inflammatory states of colonic tissues and might at least partly contribute to the pathogenesis of chronic colitis, ethanol-related colorectal cancer.

Free Research Field

臨床栄養学

Academic Significance and Societal Importance of the Research Achievements

習慣的な多量飲酒は大腸がん発症リスクを増大させる一方、その要因については未だ不明な点が多い。本研究成果より、長期アルコール摂取が結腸内にて酸化ストレス増加を誘導し、腸内細菌叢構造を変化させることを示した。これらは、結腸組織への終末糖化産物蓄積の寄与も関わっていると推察された。今後、抗酸化作用を有した毎日の食習慣アプローチより、飲酒による慢性大腸炎、がん発症予防に繋がると考える。