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Goji berry attenuates dextran sulfate sodium‐induced colitis
Author(s) -
Kang Yifei,
Xue Yansong,
Du Min,
Zhu Meijun
Publication year - 2015
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.29.1_supplement.271.1
Subject(s) - colitis , inflammatory bowel disease , berry , medicine , ulcerative colitis , lycium , gastroenterology , inflammation , diarrhea , edema , immunology , disease , biology , pathology , botany , alternative medicine
Inflammatory bowel diseases (IBD) including ulcerative colitis (UC) and Crohn's disease, are gastrointestinal disorders characterized by intestinal inflammation. Goji berry ( Lycium barbarum ), also known as wolfberry, is a traditional Chinese herbal medicine, which has long been recognized for its health beneficial effects such as antioxidative effects and diabetes prevention. Nonetheless, little is known regarding its effects in dextran sulfate sodium (DSS)‐induced colitis, a common colitis model of mice, which was investigated in this study. C57BL/6J male mice were first fed a standard rodent diet with or without 1% (w/w) goji berry for 4 weeks, then colitis was induced by supplementing 3% DSS in drinking water for 7 days, followed by a 7‐day recovery period to mimic symptoms of UC. Goji supplementation has no effects on body weight gain and feed intake in mice without DSS‐induced colitis. In DSS‐induced groups, Goji berry ameliorated body weight loss, diminished diarrhea and gross bleeding, resulting in a significantly decreased disease activity index associated with diminished DSS‐induced colon shortening. Histologically, Goji berry improved colonic edema, mucosal damage, and goblet cell depletion induced by DSS. In addition, Goji berry suppressed abnormal IL‐6 and COX2 mRNA expression, as well as apoptosis marker, active caspase‐3 content. In conclusion, for the first time, we demonstrate that dietary Goji berry supplementation confers protective effects against DSS‐induced colitis, suggesting a potential therapeutic value for IBD patients (NIH R15HD073864).