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ABSTRACT: Liver iron overload can be found in a number of different chronic liver diseases. Iron is proposed to play a role in promoting hepatic fibrosis by various mechanisms, including iron-catalyzed production of free radical and lipid peroxidation, alteration of essential biomolecules, triggering cell apoptosis and necrosis, and activation and transformation of the hepatic stellate cell into a myofibroblastic cell. Recent evidences demonstrate that the decrease of hepcidin, a 25-amino acid peptide produced by the hepatocytes, may play a significant role in promoting hepatic iron overload in various chronic liver diseases. Therefore, the supplemental hepcidin therapy may reduce liver iron concentration. Hepcidin or hepcidin-related therapeutics could find a place in the treatment of various iron overload diseases and hepatic fibrosis.
Sheng li ke xue jin zhan [Progress in physiology] 06/2010; 41(3):183-8.
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ABSTRACT: The heat and ferrous ion-activated sodium peroxydisulfate (PDS) for the oxidation of 4-chlorophenol (4-CP) was investigated. These processes are based on the generation of sulfate radicals, which are powerful oxidizing species found in nature. The effects of temperature, pH, the initial concentrations of Fe (II), PDS and citric acid on the degradation efficiencies of 4-CP were studied. The results show that the degradAtion efficiency of 4-CP is significantly enhanced as temperature increases. The degradation efficiencies of 4-CP are 2.5% and 43.5% within 4 h at 30 degrees C and 50 degrees C, respectively. Moreover, 4-CP is degraded completely at 60 degrees C. The degradation efficiency of 4-CP follows the order: pH 4.0 > pH 7.0 > pH 10.0. In the PDS/Fe (II) system, ferrous ion played an important role in generating sulfate radicals at ambient temperature. The optimum experimental condition is established and the addition of probe compounds proves the formation of sulfate radicals. Furthermore, the iron availability in the aqueous solution is manipulated with the optimum amount of citric acid, as a chelating agent. The degradation efficiency of 4-CP is 50.9% in the PDS/Fe (II)/citric acid system, which is superior to 43.5% at 50 degrees C under the same initial concentration of PDS.
Huan jing ke xue= Huanjing kexue / [bian ji, Zhongguo ke xue yuan huan jing ke xue wei yuan hui "Huan jing ke xue" bian ji wei yuan hui.] 05/2010; 31(5):1233-8.
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ABSTRACT: Iron overload induced by brain ischemia has been shown to be involved in neurodegenerative disease. Little is known about the relationship between brain ischemia and ferroportin 1 (FP1). The aims of this study are: (i) to determine whether iron accumulation in the brain is induced by cerebral hypoperfusion; and (ii) to test whether expression of FP1 is influenced by cerebral ischemia. The common carotid arteries (CCA) of rats were ligated bilaterally to induce cerebral ischemia, and the iron concentration of the cortex and hippocampus was measured by graphite furnace atomic absorption spectrometry. Iron was stained by Perl's method. The expression of FP1 mRNA and protein was shown by the reverse transcriptase polymerase chain reaction and immunohistochemical methods. The iron concentration in the cortex and hippocampus of ischemic rats had increased on day 7 (CCA7) and significantly on day 28 (CCA28) compared to control rats. More iron granules had been deposited in the cerebral cortex and hippocampus in rats with bilaterally ligated CCA on CCA7 and CCA28. In ischemic rats, FP1 expression in the cerebral cortex and hippocampus was decreased by CCA7 and this was more marked by CCA28 compared to control rats. We therefore concluded that iron deposition in the cerebral cortex and hippocampus of rats is induced by cerebral ischemia. Iron deposition may be attributed to the decrease in FP1 expression, and this inhibition of FP1 expression could be a major contributor to the formation of iron deposits in cerebral ischemia.
Journal of Clinical Neuroscience 09/2009; 16(11):1466-72. · 1.25 Impact Factor
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Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics 07/2009; 11(6):510-3.
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ABSTRACT: To explore effects of cerebral ischemia on the ceruloplasmin (Cp) expression in the cortex and hippocampus of rats.
Male Wistar rats were randomly divided into cerebral ischemia group and control group. Cerebral ischemia was induced by ligating bilateral common carotid arteries and the ischemic rats were further subgrouped according to ischemia time. The control rats received a sham operation. The expression of Cp mRNA in the cortex and hippocampus was measured by reverse transcription polymerase chain reaction (RT-PCR). The Cp expression was shown by immunohistochemistrical (streptavidin peroxidase, SP) method.
In ischemia group, the expression of Cp mRNA in the cortex and hippocampus decreased compared with that in control group (P< 0.01); and the longer rats experienced cerebral ischemia, the lower Cp mRNA expressed. By immunohistochemistry, Cp was shown expressed in the neural cells including epithelial cells of choroid plexus, ependymal cells, astrocytes of cortex and hippocampus, and vascular endothelial cells, but not in pyramidal cells and granulosa cells of cortex and hippocampus. Cp levels in the cortex and hippocampus decreased in rats suffering from cerebral ischemia for 3 d, 7 d and 28 d but not in rats exposed to ischemia for 1 d compared with that in control group (P< 0.05). Iron concentration correlated negatively with Cp expression in the cortex and hippocampus of rats exposure to ischemia (the cortex, r = -0.831, P< 0.01; the hippocampus, r = -0.809, P< 0.01).
Cerebral ischemia inhibited Cp expression in the cortex and hippocampus of rats. The decrease of Cp might be involved in iron deposition in neurons.
Neuroscience Bulletin 01/2008; 24(1):13-20. · 1.31 Impact Factor
