Oyster (Crassostrea gigas) Extract Attenuates Dextran Sulfate Sodium-Induced Acute Experimental Colitis by Improving Gut Microbiota and Short-Chain Fatty Acids Compositions in Mice

• Published in: Foods
• Main Authors: Tatsuya Ishida, Hiroyuki Matsui, Yoshikazu Matsuda, Ryota Hosomi, Takaki Shimono, Seiji Kanda, Toshimasa Nishiyama, Kenji Fukunaga, Munehiro Yoshida
• Format: Text
• Language: English
• Published: Multidisciplinary Digital Publishing Institute 2022
• Subjects: oyster extract; Crassostrea gigas; inflammatory bowel disease; experimental colitis; microbiota; short-chain fatty acid
• Online Access: https://doi.org/10.3390/foods11030373

Drugs for inflammatory bowel diseases can be associated with serious side effects, and the development of alternative candidate resources derived from natural products has attracted considerable attention. Oyster extract (OE) derived from Crassostrea gigas contains glycogen, taurine, and amino acids, and has been assigned diverse health-promoting properties. This study investigated the anti-colitis effect of OE intake on fecal microbiota and its metabolites of acute experimental colitis mouse model induced by dextran sulfate sodium (DSS). C57BL/6J mice (male) were divided into three groups: (1) American Institute of Nutrition (AIN) 93G diet + DSS-untreated, (2) AIN93G diet + DSS-treated, and (3) 5% OE diet + DSS-treated. Mice were fed each diet for 21 days, and then administered 2.5% DSS solution to induce acute colitis for 7 days. In DSS-induced colitis mice, OE decreased body weight loss and increased disease activity index during the DSS-induced period. In addition, OE tended to decrease the colon length shortening and the relative spleen weight and alleviated colonic tissue damage. Moreover, OE improved fecal short-chain fatty acids compositions and altered the structure of fecal microbiota. These results provide insight into the health-promoting property of OE in alleviating DSS-induced acute colitis, providing a basis for the development and use of functional foods.