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首页> 外文期刊>Food and Chemical Toxicology: An International Journal Published for the British Industrial Biological Research >Prophylactic role of curcumin in dextran sulfate sodium (DSS)-induced ulcerative colitis murine model.
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Prophylactic role of curcumin in dextran sulfate sodium (DSS)-induced ulcerative colitis murine model.

机译:姜黄素在硫酸葡聚糖硫酸钠(DSS)诱导的溃疡性结肠炎小鼠模型中的预防作用。

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We have addressed in this study the possible protective role of the main principle of turmeric pigment; curcumin on a murine model of ulcerative colitis (UC). Colitis was induced by administration of dextran sulfate sodium (DSS) (3% W/V) in drinking water to male Swiss albino rats for 5 consecutive days. DSS challenge induced UC model that was well characterized morphologically and biochemically. DSS produced shrinkage of colon length and increased the relative colon weight/length ratio accompanied by mucosal edema and bloody stool. Histologically, DSS produced submucosal erosions, ulceration, inflammatory cell infiltration and crypt abscess as well as epithelioglandular hyperplasia. The model was confirmed biochemically, and the test battery entailed elevated serum tumor necrosis factor (TNF-alpha) and colonic activity of myleoperoxidase (MPO). Colonic glutathione-S-transferase (GST) activity and its substrate concentration; GSH, were notably reduced, while lipid peroxidation, expressed as malondialdehyde (MDA) level, and total nitric oxide (NO) were significantly increased. Prior administration of curcumin (100mg/kg, IP) for 7 consecutive days ahead of DSS challenge mitigated the injurious effects of DSS and ameliorated all the altered biochemical parameters. These results suggest that curcumin could possibly have a protective role in ulcerative colitis probably via regulation of oxidant/anti-oxidant balance and modulation of the release of some inflammatory endocoids, namely TNF-alpha and NO.
机译:我们已经在这项研究中解决了姜黄颜料主要原理的可能的保护作用。姜黄素对溃疡性结肠炎(UC)小鼠模型的作用。连续5天对瑞士白化病雄性大鼠服用饮用水中的右旋糖酐硫酸钠(DSS)(3%W / V)诱发结肠炎。 DSS挑战诱导的UC模型在形态和生化上都有很好的表征。 DSS使结肠长度缩小,并增加相对结肠重量/长度比,并伴有粘膜水肿和血便。在组织学上,DSS引起粘膜下糜烂,溃疡,炎性细胞浸润和隐窝脓肿以及上皮腺增生。该模型已经过生化确认,测试电池需要升高血清肿瘤坏死因子(TNF-alpha)和髓过氧化物酶(MPO)的结肠​​活性。结肠谷胱甘肽-S-转移酶(GST)活性及其底物​​浓度; GSH明显降低,而脂质过氧化表示为丙二醛(MDA)水平和总一氧化氮(NO)显着增加。在DSS攻击之前连续7天预先给予姜黄素(100mg / kg,IP)可减轻DSS的伤害作用并改善所有改变的生化参数。这些结果表明姜黄素可能通过调节氧化剂/抗氧化剂的平衡以及调节某些炎症性内生菌类TNF-α和NO的释放而在溃疡性结肠炎中具有保护作用。

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