Department of Biochemistry, Christian Medical College, Vellore, Tamil Nadu, India.
Br J Nutr. 2012 Dec 14;108(11):1994-2001. doi: 10.1017/S0007114512000189. Epub 2012 Feb 24.
In order to understand better the molecular mechanisms involved in the pathogenesis of anaemia of inflammation, we carried out a time-course study on the effects of turpentine-induced acute and chronic inflammation on duodenal proteins involved in Fe absorption in mice. Expression levels of these proteins and hepatic hepcidin and serum Fe levels were determined in inflamed mice. In acutely inflamed mice, significantly increased expression of ferritin was the earliest change observed, followed by decreased divalent metal transporter 1 expression in the duodenum and increased hepcidin expression in the liver. Ferroportin expression increased subsequently, despite high levels of hepcidin. Hypoferraemia, which developed at early time periods studied, was followed by increased serum Fe levels at later points. The present results thus show that acute inflammation induced several changes in the expression of proteins involved in duodenal Fe absorption, contributing to the development of hypoferraemia. Resolution of inflammation caused attenuation of many of these effects. Effects in chronically inflamed mice were less consistent. The present results also suggest that inflammation-induced increases in ferritin appeared to override the effects of hepcidin on the expression levels of ferroportin in enterocytes.
为了更好地理解炎症性贫血发病机制中的分子机制,我们对松节油诱导的急性和慢性炎症对小鼠十二指肠中铁吸收相关蛋白的影响进行了时间进程研究。在炎症小鼠中测定了这些蛋白以及肝组织中hepcidin 和血清铁水平的表达水平。在急性炎症小鼠中,最早观察到的变化是铁蛋白表达显著增加,随后是十二指肠中二价金属转运蛋白 1 的表达减少,肝组织中 hepcidin 的表达增加。尽管 hepcidin 水平较高,但随后铁蛋白的表达增加。在研究的早期阶段出现的低铁血症随后在后期出现血清铁水平升高。因此,这些结果表明急性炎症引起了十二指肠中铁吸收相关蛋白表达的几种变化,导致低铁血症的发生。炎症的消退导致许多这些效应减弱。慢性炎症小鼠的影响则不太一致。这些结果还表明,炎症诱导的铁蛋白增加似乎超过了 hepcidin 对肠细胞中铁蛋白表达水平的影响。