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Objective To investigate the effect of Ginkgo biloba extract on serum divalent metal transporter1 ( DMT1 ) , glucose regulated protein 75(grp75) and nerve function in patients with Parkinson disease.Methods 38 cases of patients loith parkinson disease according to different drugs were divided into experimental group and control group, 19 cases in each group.Control group was treated with levodopa and Benserazide tablet, experimental group on the basis of control group, was given Ginkgo biloba extract tablets, treatment for 4 weeks.After treatment, DMT1, grp75 and cognitive function of all patients in substantia nigra were detected.ResuIts Compared with before treatment, two groups of patients with lower DMT1 level (P<0.05), compared with control group, experimental group of patients with lower DMT1 levels (P<0.05).Compared with pre-treatment, two groups of patients grp75 level was higher (P<0.05), compared with control group, experimental group after treatment grp75 level was higher (P<0.05).Compared with before treatment, the two groups of patients with MoCA scores were higher (P<0.05), HAMD scores were lower (P<0.05).Compared with control group, experimental group after treatment MoCA scores were higher (P<0.05), HAMD scores were lower (P<0.05).ConcIusion Ginkgo biloba extract can significantly reduce the level of DMT1 in the substantia nigra of Parkinson patients, increase the level of grp75, and improve the cognitive function.
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<p><b>OBJECTIVE</b>To investigate the multiple iron metabolism-related genes expression, its regulation by iron and the expression correlation among the genes in rat tissues.</p><p><b>METHODS</b>Two groups (n=30) of Sprague-Dawley female weanling rats were fed with a control diet and an iron deficient diet respectively for 4 weeks. All rats were then sacrificed, and blood and tissue samples were collected. The routine blood examination was performed with a veterinary automatic blood cell analyzer. Elemental iron levels in liver, spleen and serum were determined by atomic absorption spectrophotometry. The mRNA expression of genes was detected by real-time fluorescence quantitative PCR.</p><p><b>RESULTS</b>After 4 weeks, the hemoglobin (Hb) level and red blood cell (RBC) count were significantly lower in the iron deficient group compared with those in the control group. The iron levels in liver, spleen and serum in the iron deficient group were significantly lower than those in the control group. In reference to small intestine, the relative expression of each iron-related gene varied in the different tissues. Under the iron deficiency, the expression of these genes changed in a tissue-specific manner. The expression of most of the genes significantly correlated in intestine, spleen and lung, but few correlated in liver, heart and kidney.</p><p><b>CONCLUSION</b>Findings from our study provides new understandings about the relative expression, regulation by iron and correlation among the mRNA expressions of transferrin receptors 1 and 2, divalent metal transporter 1, ferritin, iron regulation proteins 1 and 2, hereditary hemochromatosis protein, hepcidin, ferroportin 1 and hephaestin in intestine, liver, spleen, kidney, heart, and lung of rat.</p>
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Animales , Ratas , Ferritinas , Sangre , Expresión Génica , Hepcidinas , Hierro , Hígado , Metabolismo , Ratas Sprague-DawleyRESUMEN
Iron and zinc interact at the enterocyte during absorption, but the mechanism(s) remain elusive. The aim was, therefore, to understand the mechanism of interaction using kinetic analyses of iron and zinc uptake, individually and in combination under normal and altered cellular mineral concentrations in human intestinal Caco-2 cell line. Striking differences in kinetic parameters were observed between iron and zinc uptake. Iron uptake followed a two-component model, while zinc uptake followed a three-component model. Iron uptake had a Km of 3.6 µM and Vmax of 452 pmol/mg protein/min, while zinc uptake had a Km of 42 µM and Vmax of 3.09 pmol/mg protein/min. Zinc dose-dependently inhibited iron uptake through mixed-inhibition but iron marginally increased zinc uptake. Cellular zinc repletion doubled iron uptake and eliminated inhibition, but zinc depletion decreased iron uptake. Iron pre-treatment had no effect on zinc uptake. Based on these results, a two-transporter model of iron uptake, comprising the apical iron uptake transporter divalent metal ion transporter-1 (DMT-1) and an unknown putative transporter was derived. This model for DMT-1 was verified by immunoblotting. These results implied that cellular zinc status profoundly influenced iron uptake and its interactions with zinc during uptake. DMT-1 might not simultaneously transport iron and zinc, providing a mechanistic basis for observed interactions.
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Animales , Transporte Biológico , Células CACO-2 , Proteínas de Transporte de Catión/metabolismo , Relación Dosis-Respuesta a Droga , Enterocitos/metabolismo , Regulación de la Expresión Génica , Humanos , Absorción Intestinal , Intestinos/metabolismo , Hierro/química , Cinética , Modelos Biológicos , Ratas , Zinc/químicaRESUMEN
Objective:To observe the effect of high zinc concentrations on contents of iron and zinc and expression of their regulating mRNA in Caco-2 cells.Methods: Caco-2 cells were used as model of human small intestinal enterocytes and were treated for 24 h with 4,50,100 and 200 ?mol/L of zinc.The zinc and iron contents were determined by atom absorption spectrophotography and the expression of DMT1,IREG1,ZnT1 and hZIP4 mRNA were determined by RT-PCR(the level of GAPDH was taken as internal control).Results: The zinc content in Caco-2 cells was increased 24 h after treatment with zinc,and reached the peak when exposed to 50 ?mol/L zinc.The iron content decreased with the increase of zinc concentration.Zinc supplement increased the expressions of DMT1,IREG1 and ZnT1 mRNA but decreased the expression of hZIP4 mRNA.Conclusion: It is suggested that zinc supplement can increase the contents of zinc but decrease the contents of iron in Caco-2 cells.There may be interactions between iron and zinc in the intestinal lumen.