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Studies of gut mucosal protein synthesis in a non-steroidal anti-inflammatory drug (NSAID) model of inflammatory bowel disease.

机译:在炎症性肠病的非甾体抗炎药(NSAID)模型中研究肠粘膜蛋白合成。

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摘要

The extent to which defects in protein synthesis occurred in an experimental indomethacin induced rat model of nonsteroidal enteropathy has been examined. Male rats (nine) were fed indomethacin (8 mg/kg/day) for three days mixed with a powdered form of chow. The control group of rats (nine) were fed the same diet for three days without indomethacin. After the feeding period, both groups were fed a normal solid diet for four days. At the end of this period, the fractional rates of intestinal protein synthesis was determined by the 'flooding dose' technique. The mucosal protein, RNA and DNA contents in the proximal ileum of animals with enteropathy were not significantly different from controls (p greater than 0.05). Experimental enteropathy induced selective increases in the fractional rates of protein synthesis (26% increase, p less than 0.03) and RNA activities (23% increase, p less than 0.04). There were no significant changes in any of these variables in the duodenum (p greater than 0.05 in all instances). These changes may partly reflect the activity of those processes responsible for the pathogenic changes in NSAID enteropathy.
机译:已经研究了在吲哚美辛诱导的非甾体肠病大鼠模型中蛋白质合成缺陷的程度。给雄性大鼠(9只)喂食消炎痛(8 mg / kg /天),并与粉状食物混合三天。对照组(9只)在不服用消炎痛的情况下,以相同的饮食喂养了3天。喂食期过后,两组均以正常固体饮食喂食四天。在此期间结束时,肠蛋白质合成的分数速率通过“溢流剂量”技术确定。肠病动物回肠近端回肠的黏膜蛋白,RNA和DNA含量与对照组无显着差异(p大于0.05)。实验性肠病导致蛋白质合成分数速率的选择性增加(增加26%,p小于0.03)和RNA活性(增加23%,p小于0.04)。十二指肠中的所有这些变量均无显着变化(在所有情况下,p均大于0.05)。这些变化可能部分反映了引起NSAID肠病致病性变化的那些过程的活动。

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