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姜黄素在葡聚糖硫酸钠(DSS)诱导的溃疡性结肠炎小鼠模型中的预防作用。

Prophylactic role of curcumin in dextran sulfate sodium (DSS)-induced ulcerative colitis murine model.

作者信息

Arafa Hossam M M, Hemeida Ramadan A, El-Bahrawy Ali I M, Hamada Farid M A

机构信息

Department of Pharmacology and Toxicology, Faculty of Pharmacy, Al-Azhar University, Nasr City, Cairo 11231, Egypt.

出版信息

Food Chem Toxicol. 2009 Jun;47(6):1311-7. doi: 10.1016/j.fct.2009.03.003. Epub 2009 Mar 12.

Abstract

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.

摘要

在本研究中,我们探讨了姜黄色素的主要成分姜黄素对溃疡性结肠炎(UC)小鼠模型可能具有的保护作用。通过向雄性瑞士白化病大鼠连续5天饮用含3%(W/V)葡聚糖硫酸钠(DSS)的水来诱导结肠炎。DSS激发诱导的UC模型在形态和生化方面都有很好的表征。DSS导致结肠长度缩短,结肠相对重量/长度比增加,伴有黏膜水肿和血便。组织学上,DSS导致黏膜下糜烂、溃疡、炎性细胞浸润和隐窝脓肿以及上皮腺增生。该模型通过生化方法得到证实,检测指标包括血清肿瘤坏死因子(TNF-α)升高和结肠髓过氧化物酶(MPO)活性升高。结肠谷胱甘肽-S-转移酶(GST)活性及其底物浓度(谷胱甘肽,GSH)显著降低,而以丙二醛(MDA)水平表示的脂质过氧化和总一氧化氮(NO)显著增加。在DSS激发前连续7天预先给予姜黄素(100mg/kg,腹腔注射)减轻了DSS的损伤作用,并改善了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/抗氧化平衡以及调节某些炎性内分泌物(即TNF-α和NO)的释放,对溃疡性结肠炎具有保护作用。

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