Laboratory investigation; a journal of technical methods and pathology
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Comparative Study
Ferroportin-1 is a 'nuclear'-negative acute-phase protein in rat liver: a comparison with other iron-transport proteins.
Liver is the central organ of iron metabolism. During acute-phase-response (APR), serum iron concentration rapidly decreases. The current study aimed to compare expression and localization of iron transport protein ferroportin-1 (Fpn-1) and of other iron import proteins after experimental tissue damage induced by injecting turpentine oil in the hind limbs of rats and mice. ⋯ Moreover, western blot analysis of cell lysate of IL-6-treated hepatocytes detected, as expected, an increase of a2-macroglobulin (positive acute-phase protein), whereas albumin (negative acute-phase protein) and Fpn-1 were downregulated. Our results demonstrate that liver behaves as a 'sponge' for iron under acute-phase conditions, and Fpn-1 behaves as a negative acute-phase protein in rat hepatocytes mainly, but not exclusively, because of the effect of IL-6. These changes could explain iron retention in the cytoplasm and in the nucleus of hepatocytes during APR.
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To determine whether the presence of Matrix metalloproteinases (MMPs) is associated with acute lung injury following cardiopulmonary bypass (CPB), we evaluated the activity and gene expression of matrix metalloproteinases-9 (MMP-9) and tissue inhibitor of metalloproteinase-1 (TIMP-1) of lungs using rat model of CPB. Adult male Sprague-Dawley rats were randomly divided into three groups: Group I (underwent cannulation + heparinization only); group II (underwent 60 min of normothermic CPB); and group III (underwent 60 min of normothermic of CPB, which rats received doxycycline treat by filling stomach 1 week ahead of CPB). Lung injury was evaluated histologically. ⋯ We concluded MMP-9 might have an important role in acute lung injury following CPB. TIMP-1 increased in the rats treated with doxycycline ahead and might compensate for the activity of MMP-9. The doxycycline might have the protective effect against acute lung injury following CPB.