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肥大细胞在小鼠实验性结肠炎发病机制中缺乏关键作用。

Lack of crucial role of mast cells in pathogenesis of experimental colitis in mice.

作者信息

Minocha A, Thomas C, Omar R

机构信息

Department of Medicine, University of Louisville, Kentucky, USA.

出版信息

Dig Dis Sci. 1995 Aug;40(8):1757-62. doi: 10.1007/BF02212698.

Abstract

Mast cell alterations have been implicated in the pathogenesis of chronic ulcerative colitis (UC). We studied the effect of mast cell deficiency of the severity of inflammation in a murine model of colitis. Colitis was induced in mice using dextran sodium sulfate (DSS). Mast-cell-deficient mice (WBB6F1/J-W/WV; N = 17) and normal littermates (WBB6F1/J-+/+; N = 17) were administered DSS 4% w/v for seven days, then water alone for one week, followed by 5% DSS for six days. Animals were sacrificed at the end of the protocol. Segments of proximal, mid-, and distal colon of each animal were processed for histopathological examination. Mortality and morbidity (diarrhea and weight loss) for each group were assessed. There was no significant difference between the two groups in either their clinical parameters (mortality and morbidity) or the severity of colitis as graded histopathologically. Our findings suggest that mast cells are not crucial for the development of DSS-induced colitis.

摘要

肥大细胞改变与慢性溃疡性结肠炎(UC)的发病机制有关。我们在小鼠结肠炎模型中研究了肥大细胞缺陷对炎症严重程度的影响。使用葡聚糖硫酸钠(DSS)诱导小鼠发生结肠炎。给肥大细胞缺陷小鼠(WBB6F1/J-W/WV;N = 17)和正常同窝小鼠(WBB6F1/J-+/+;N = 17)给予4% w/v的DSS,持续7天,然后仅给予水1周,接着给予5% DSS,持续6天。在实验方案结束时处死动物。对每只动物的近端、中段和远端结肠段进行组织病理学检查。评估每组的死亡率和发病率(腹泻和体重减轻)。两组在临床参数(死亡率和发病率)或组织病理学分级的结肠炎严重程度方面均无显著差异。我们的研究结果表明,肥大细胞对DSS诱导的结肠炎的发展并不关键。

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