ABSTRACT
ObjectiveTo investigate the effects of lipopolysaccharide (LPS) on mRNA expression of iron metabolism related genes. Methods Ten male mice (2 months) were injected intraperitoneally with lipopolysaccharide(0.5 μg/g). After 6 hours, mice were sacrificed and then sera, liver and spleen were collected. The mice blood routine was measured. The serum iron and total iron binding capacity (TIBC) were determined with reagent kit. The quasi-quantitative reverse transcription polymerase chain reaction (RT-PCR) was performed for mRNA of hepatic hepcidin(HP), ferroportin1(Fpn1), transferrin receptor 1(TfR1) and spleenic HP, Fpn1 and interleukin-6(IL-6). Results The serum iron and TIBC were reduced in mice injected LPS, which exhibited mild anemia(P＜0.05) . LPS can increase the expression of hepatic hepcidin and decrease Fpn1 and TfR1 in liver after LPS administration 6 hours(P＜0.05). In spleen, IL-6 was upregulated and Fpn1 downregulated(P＜0.05). Conclusion LPS can influence serum iron through regulating the mRNA expression of hepatic and spleenic iron metabolism related genes, such as HP, Fpn1 and TfR1.
ABSTRACT
OBJECTIVE: In order to understand the effect of stimulator of Fe transport(SFT) on Fe metabolism and its abnormality(absence or overloading),this study reviews the research development of SFT at home and abroad and focused on the relationship among expression,structure,physiological function,expressing controlling and expressing abnormality with brain iron metabolism.DATA SOURCES: Electronic literature search of NCBI related to SFT was performed using the terms "stimulator of iron transport" or "stimulator of Fe transport",and the language was restricted in English. And simultaneously CNKI database was searched with the word "brain iron metabolism" and"stimulator of Fe transport" in Chinese from January 1997 to October 2004.STUDY SELECTION: Articles that reported the structure,expression regulation of SFT and its relationship to brain iron metabolism diseases were included.DATA EXTRACTION: Twenty pieces of SFT-related literatures and 1300pieces of literatures related to brain iron metabolism were found,among which 21 pieces were included.DATA SYNTHESIS: From the 21 pieces of literatures,the structure,distribution,biological function,expression regulation of SFT and its relationship with brain iron metabolism were mainly discussed.CONCLUSION: SFT can stimulate both transferrin- and nontransferrin-bound iron uptake. The expression of SFT can be regulated transcriptionally and post-transcriptionally,mainly regulated in response to different cellular iron levels. So SFT plays an important role in brain iron metabolism.
ABSTRACT
The understanding of iron metabolism in humans, especially of its mechanism involved in controlling iron absorption in the proximal small intestine, is of great importance since diseases associated with iron deficiency or overload are very common worldwide. Recent study on hepcidin which is senthesized by liver has showed that this originally identified as a circulating antimicrobial peptide is a putative iron regulatory hormone. It plays a central role in the regulation of small intestine iron absorption and body iron homeostasis. The increased expression of hepcidin in the liver, induced by inflammation, might be an initial cause of the anemia of infection or chronic diseases and the iron-overload diseases might be tightly associated with the decreased hepcidin expression in the liver.
ABSTRACT
AIM: To investigate the role of transferrin/transferrin receptor system in transferrin-bound Yb 2 (Yb 2Tf) uptake by U-87 MG cells and the effect of transferrin-bound and -free Yb 2 on proliferation of U-87 MG cells. METHODS: Cell culture and ICP-MS measurement of Yb 2. RESULTS: Yb 2Tf uptake by U-87 MG cells increased with the concentrations of Yb 2Tf, and reached saturation as the concentration in the incubation medium was raised to about 2 ?mol/L. Also, Yb 2 uptake by the cells increased with increase of the mole ratio (Yb 2: apoTf), reaching a maximum at 1.5 mole ratio. Yb 2Tf in 0.4 ?mol/L significantly inhibited proliferation of U-87 MG cells, however, 10 ?mol/L Yb 3+ had no significant effect on proliferation of the cells. CONCLUSION: The uptake of Yb 2 by U-87 MG cells might be mediated by transferrin/transferrin receptor system. Transferrin-bound but not transferrin-free Yb 2 could significantly inhibit proliferation of U-87 MG cells.
ABSTRACT
Objective To study the influence of ion concentration change out of cells on calcium transportation and the relationship between the rising of calcium concentration in the Caco-2 cells and its apoptosis to offer the theoretical and experimental bases for clinical study and digestive tract physiology and patholoogy. Methods Confocal laser scanning microscope(CLSM) and flow cytometry(FCM) were used in this study. Results (1) Diversion of Ca 2+ into cells was increased with the decrease of Fe 3+ concentration out of Caco-2 cells(the final consistence of DFO was 100-300??mol/L),but was hindered with the increase of Fe 3+ concentration out of them(the final consistence fo FAC was 10-100??mol/L) as observed under CLSM; (2) The cell state was fine and its viability was more than 90% as observed under CLSM after treated by A 23187 and Fluo-3/AM(examined with FDA);(3) The Ca 2+ concentration in the Caco-2 cells was increased by A 23187 and this function was dose depended.The Caco-2 cell apoptosis was induced by the increase of Ca 2+ in cells,which was examined with FCM.Conclusion The Ca 2+ transportation was increased with the decrease of Fe 3+ concentration out of Caco-2 cells but was hindered with the increase of Fe 2+ concentration out of them.The Caco-2 cell apoptosis was induced by the increase of Ca 2+ concentration in them.