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자료유형
학술저널
저자정보
Taya, Sirinya (Department of Molecular Pathology, Osaka City University Graduate School of Medicine) Kakehashi, Anna (Department of Molecular Pathology, Osaka City University Graduate School of Medicine) Wongpoomchai, Rawiwan (Department of Biochemistry, Faculty of Medicine, Chiang Mai University) Gi, Min (Department of Molecular Pathology, Osaka City University Graduate School of Medicine) Ishii, Naomi (Department of Molecular Pathology, Osaka City University Graduate School of Medicine) Wanibuchi, Hideki (Department of Molecular Pathology, Osaka City University Graduate School of Medicine)
저널정보
아시아태평양암예방학회 Asian Pacific journal of cancer prevention : APJCP Asian Pacific journal of cancer prevention : APJCP 제17권 제4호
발행연도
2016.1
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2,235 - 2,245 (11page)

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Ulcerative colitis (UC) results from colonic epithelial barrier defects and impaired mucosal immune responses. In this study, we aimed to investigate the modifying effects of a Spirogyra neglecta extract (SNE), a polysaccharide extract (PE) and a chloroform fraction (CF) on dextran sodium sulfate (DSS)-induced colitis in mice and to determine the mechanisms. To induce colitis, ICR mice received 3% DSS in their drinking water for 7 days. Seven days preceding the DSS treatment, oral administration of SNE, PE and CF at doses of 50, 25 and 0.25 mg/kg body weight (low dose), 200, 100 and 1 mg/kg body weight (high dose) and vehicle was started and continued for 14 days. Histologic findings showed that DSS-induced damage of colonic epithelial structure and inflammation was attenuated in mice pre-treated with SNE, PE and CF. Furthermore, SNE and PE significantly protected colonic epithelial cells from DSS-induced cell cycle arrest, while SNE, PE and CF significantly diminished apoptosis. Proteome analysis demonstrated that SNE and PE might ameliorate DSS-induced colitis by inducing antioxidant enzymes, restoring impaired mitochondria function, and regulating inflammatory cytokines, proliferation and apoptosis. These results suggest that SNE and PE could prevent DSS-induced colitis in ICR mice by protection against and/or aiding recovery from damage to the colonic epithelium, reducing ROS and maintaining normal mitochondrial function and apoptosis.

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