姜黄素
结肠炎
炎症
促炎细胞因子
炎症性肠病
细胞因子
肠粘膜
药理学
化学
医学
免疫学
病理
内科学
疾病
作者
Ken Sugimoto,Hiroyuki Hanai,Kotaro Tozawa,Taiki Aoshi,Masato Uchijima,Toshi Nagata,Yukio Koide
出处
期刊:Gastroenterology
[Elsevier BV]
日期:2002-12-01
卷期号:123 (6): 1912-1922
被引量:227
标识
DOI:10.1053/gast.2002.37050
摘要
Background & Aims: Curcumin is known to have a variety of pharmacologic effects, including antitumor, anti-inflammatory, and anti-infectious activities. The pleiotropic effects of curcumin are attributable at least in part to inhibition of transcriptional factor nuclear factor κB (NF-κB). However, the effect of curcumin on intestinal inflammation has hitherto not been evaluated. The aim of this study was to determine whether treatment with curcumin prevents and ameliorates colonic inflammation in a mouse model of inflammatory bowel disease. Methods: Mice with trinitrobenzene sulfonic acid (TNBS)-induced colitis were treated with 0.5%, 2.0%, or 5.0% curcumin in the diet, and changes in body weight together with histologic scores were evaluated. Colonic T-cell subsets were characterized, and NF-κB in colonic mucosa was detected by immunohistochemistry. NF-κB activity in the colonic mucosa was evaluated using electrophoretic mobility shift assay. Cytokine messenger RNA expression in colonic tissue was assessed by semiquantitative reverse-transcription polymerase chain reaction. Results: Treatment of mice with curcumin prevented and improved both wasting and histopathologic signs of TNBS-induced colonic inflammation. Consistent with these findings, CD4+ T-cell infiltration and NF-κB activation in colonic mucosa were suppressed in the curcumin-treated group. Suppression of proinflammatory cytokine messenger RNA expression in colonic mucosa was also observed. Conclusions: This study has shown for the first time that treatment with curcumin can prevent and improve murine experimental colitis. This finding suggests that curcumin could be a potential therapeutic agent for the treatment of patients with inflammatory bowel disease.GASTROENTEROLOGY 2002;123:1912-1922
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