The Department of Surgery, University of Cincinnati, OH 45267, USA.
Biol Trace Elem Res. 2011 Jul;142(1):47-54. doi: 10.1007/s12011-010-8743-9. Epub 2010 Jun 11.
Copper deficiency can cause a host of major cardiovascular complications including an augmented inflammatory response through effects on both neutrophils and the microvascular endothelium. In the present study, we evaluated the effect of marginal copper deficiency on the neutrophilic response to hepatic ischemia/reperfusion injury, a condition that induces an inflammatory response. Male weanling Sprague-Dawley rats were fed purified diets which were either copper-adequate (6.3 mg/kg) or copper-marginal (1.62 mg/kg) for 4 weeks prior to undergoing 90 min of partial hepatic ischemia followed by 8 h of reperfusion. Liver injury was assessed by serum levels of alanine aminotransferase and by liver histology. Liver neutrophil accumulation was determined by tissue myeloperoxidase content. There was no significant difference in liver injury between copper-adequate and copper-marginal rats. However, liver neutrophil accumulation was significantly increased in copper-marginal rats. These findings were confirmed histologically. Liver expression of the adhesion molecule, intercellular adhesion molecule-1 (ICAM-1), was increased in copper-marginal rats compared to copper-adequate rats. The results suggest that neutrophil accumulation is increased through enhanced ICAM-1 expression in liver of copper-marginal rats after ischemia/reperfusion, but that this does not result in increased liver injury.
铜缺乏可引起一系列主要心血管并发症，包括通过对中性粒细胞和微血管内皮的影响增强炎症反应。在本研究中，我们评估了边缘性铜缺乏对肝缺血/再灌注损伤中性粒细胞反应的影响，这种情况会引起炎症反应。雄性断奶 Sprague-Dawley 大鼠在接受 90 分钟部分肝缺血和 8 小时再灌注之前，用含有足够（6.3mg/kg）或边缘（1.62mg/kg）铜的纯化饮食喂养 4 周。通过血清丙氨酸转氨酶水平和肝组织学评估肝损伤。通过组织髓过氧化物酶含量确定肝中性粒细胞积聚。铜充足和铜边缘大鼠之间的肝损伤无明显差异。然而，铜边缘大鼠的肝中性粒细胞积聚明显增加。这些发现得到了组织学的证实。与铜充足大鼠相比，铜边缘大鼠肝中的粘附分子细胞间粘附分子-1（ICAM-1）表达增加。结果表明，缺血/再灌注后铜边缘大鼠肝内中性粒细胞积聚增加是通过增强 ICAM-1 表达引起的，但这并不会导致肝损伤增加。
