首页> 外文期刊>American Journal of Physiology >Augmented metalloproteinase activity and acute lung injury in copper-deficient rats.
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Augmented metalloproteinase activity and acute lung injury in copper-deficient rats.

机译:铜缺乏大鼠的金属蛋白酶活性增强和急性肺损伤。

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摘要

Dietary copper is required for normal function of >30 mammalian enzyme systems. Copper deficiency causes a number of cardiovascular defects as well as impaired immune cell function. Little is known regarding the effects of copper deficiency on acute inflammatory responses, but this topic is relevant because many members of the Western population receive less than the recommended dietary allowance of copper. In the current studies, we investigated the effects of dietary copper deficiency on acute lung injury induced by intrapulmonary deposition of IgG immune complexes. Weanling male Long-Evans rats were fed diets either adequate (5.6 microg/g) or deficient (0.3 microg/g) in copper. IgG immune complex lung injury was greatly increased in copper-deficient rats as determined by lung vascular leakage of albumin and histopathology. However, no change was observed in either the lung content of tumor necrosis factor-alpha or lung neutrophil accumulation. Lungs from copper-deficient rats had much higher levels of matrix metalloproteinase (MMP)-2 and MMP-9 than did copper-adequate control animals. This increased activity was not attributable to alveolar macrophages or neutrophils. These data suggest that the augmented lung injury caused by copper deficiency is due to increased pulmonary MMP-2 and MMP-9 activity and not a generalized amplification of the inflammatory response.
机译:膳食铜是> 30种哺乳动物酶系统正常功能所必需的。铜缺乏会导致许多心血管疾病以及免疫细胞功能受损。关于铜缺乏对急性炎症反应的影响知之甚少,但是这个话题是有意义的,因为许多西方人群的铜摄入量少于建议的饮食摄入量。在当前的研究中,我们调查了饮食中铜缺乏对IgG免疫复合物肺内沉积诱导的急性肺损伤的影响。给断奶的雄性Long-Evans大鼠喂食足够(5.6 microg / g)或缺乏(0.3 microg / g)的铜。 IgG免疫复合物肺损伤在铜缺乏的大鼠中大大增加,这是由白蛋白的肺血管渗漏和组织病理学确定的。但是,无论是肿瘤坏死因子-α的肺含量还是肺中性粒细胞积聚都没有观察到变化。与铜充足的对照动物相比,缺铜大鼠的肺中基质金属蛋白酶(MMP)-2和MMP-9的含量高得多。这种增加的活性不归因于肺泡巨噬细胞或嗜中性粒细胞。这些数据表明,由铜缺乏引起的肺损伤加剧是由于肺MMP-2和MMP-9活性增加,而不是炎症反应的普遍性增强。

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