Sugimoto Ken, Hanai Hiroyuki, Tozawa Kotaro, Aoshi Taiki, Uchijima Masato, Nagata Toshi, Koide Yukio
First Department of Internal Medicine, Hamamatsu University School of Medicine, Japan.
Gastroenterology. 2002 Dec;123(6):1912-22. doi: 10.1053/gast.2002.37050.
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 kappaB (NF-kappaB). 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.
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-kappaB in colonic mucosa was detected by immunohistochemistry. NF-kappaB 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.
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-kappaB activation in colonic mucosa were suppressed in the curcumin-treated group. Suppression of proinflammatory cytokine messenger RNA expression in colonic mucosa was also observed.
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.
姜黄素具有多种药理作用,包括抗肿瘤、抗炎和抗感染活性。姜黄素的多效性作用至少部分归因于对转录因子核因子κB(NF-κB)的抑制。然而,姜黄素对肠道炎症的影响迄今尚未得到评估。本研究的目的是确定姜黄素治疗是否能预防和改善炎症性肠病小鼠模型中的结肠炎症。
用三硝基苯磺酸(TNBS)诱导结肠炎的小鼠在饮食中给予0.5%、2.0%或5.0%的姜黄素,评估体重变化和组织学评分。对结肠T细胞亚群进行表征,并通过免疫组织化学检测结肠黏膜中的NF-κB。使用电泳迁移率变动分析评估结肠黏膜中的NF-κB活性。通过半定量逆转录聚合酶链反应评估结肠组织中细胞因子信使RNA的表达。
用姜黄素治疗小鼠可预防并改善TNBS诱导的结肠炎症的消瘦和组织病理学症状。与这些发现一致,姜黄素治疗组结肠黏膜中的CD4(+) T细胞浸润和NF-κB激活受到抑制。还观察到结肠黏膜中促炎细胞因子信使RNA表达受到抑制。
本研究首次表明,姜黄素治疗可预防和改善小鼠实验性结肠炎。这一发现表明,姜黄素可能是治疗炎症性肠病患者的潜在治疗药物。