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Curcumin the major component of food flavour turmeric reduces mucosal injury in trinitrobenzene sulphonic acid-induced colitis

机译:姜黄素是食品姜黄的主要成分可减少三硝基苯磺酸引起的结肠炎的粘膜损伤

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摘要

class="enumerated" style="list-style-type:decimal">Inflammmatory bowel disease (IBD) is characterized by oxidative and nitrosative stress, leucocyte infiltration and upregulation of proinflammatory cytokines. In this study, we have investigated the protective effects of curcumin, an anti-inflammatory and antioxidant food derivative, on 2,4,6- trinitrobenzene sulphonic acid-induced colitis in mice, a model for IBD.Intestinal lesions (judged by macroscopic and histological score) were associated with neutrophil infiltration (measured as increase in myeloperoxidase activity in the mucosa), increased serine protease activity (may be involved in the degradation of colonic tissue) and high levels of malondialdehyde (an indicator of lipid peroxidation).Dose–response studies revealed that pretreatment of mice with curcumin (50 mg kg−1 daily i.g. for 10 days) significantly ameliorated the appearance of diarrhoea and the disruption of colonic architecture. Higher doses (100 and 300 mg kg−1) had comparable effects.In curcumin-pretreated mice, there was a significant reduction in the degree of both neutrophil infiltration (measured as decrease in myeloperoxidase activity) and lipid peroxidation (measured as decrease in malondialdehyde activity) in the inflamed colon as well as decreased serine protease activity.Curcumin also reduced the levels of nitric oxide (NO) and O2 associated with the favourable expression of Th1 and Th2 cytokines and inducible NO synthase. Consistent with these observations, nuclear factor-κB activation in colonic mucosa was suppressed in the curcumin-treated mice.These findings suggest that curcumin or diferuloylmethane, a major component of the food flavour turmeric, exerts beneficial effects in experimental colitis and may, therefore, be useful in the treatment of IBD.
机译:class =“ enumerated” style =“ list-style-type:decimal”> <!-list-behavior =枚举前缀-word = mark-type = decimal max-label-size = 0-> 炎症性肠病(IBD)的特征是氧化应激和亚硝化应激,白细胞浸润以及促炎性细胞因子的上调。在这项研究中,我们研究了姜黄素(一种抗炎和抗氧化剂的食物衍生物)对2,4,6-三硝基苯磺酸诱导的IBD模型小鼠结肠炎的保护作用。 肠病变(通过宏观和组织学评分判断)与中性粒细胞浸润(以粘膜中髓过氧化物酶活性的增加来衡量),丝氨酸蛋白酶活性的增加(可能与结肠组织的降解有关)和高水平的丙二醛(指标)有关。 剂量反应研究表明,姜黄素预处理小鼠(每天ig每天50 mg kg -1 ig 10天)可明显改善腹泻的症状,并减轻腹泻的发生。破坏结肠结构。更高的剂量(100和300 mg kg −1 )具有可比的效果。 在姜黄素预处理的小鼠中,中性粒细胞浸润的程度均显着降低(按发炎的结肠中的髓过氧化物酶活性降低)和脂质过氧化(以丙二醛活性降低来衡量)以及丝氨酸蛋白酶活性降低。 姜黄素还降低了一氧化氮(NO)和O2 -与Th1和Th2细胞因子的良好表达以及可诱导的NO合酶有关。与这些观察结果一致,姜黄素处理的小鼠结肠黏膜中的核因子-κB活化受到抑制。 这些发现表明,姜黄素或二铁酰甲烷是姜黄的主要成分,在姜黄素中发挥有益作用。实验性结肠炎,因此可能可用于治疗IBD。

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