AIM： To assess the correlation between the serum hep-cidin-25 level and left ventricular mass index.METHODS： This study was a cross-sectional study conducted between March 2009 and April 2010. Demo-graphic and bioch...AIM： To assess the correlation between the serum hep-cidin-25 level and left ventricular mass index.METHODS： This study was a cross-sectional study conducted between March 2009 and April 2010. Demo-graphic and biochemical data, including the serum hep-cidin-25 level, were collected for chronic kidney disease （CKD） patients. Two-dimensional echocardiography was performed to determine the left ventricle mass （LVM）, left ventricular mass index （LVMI）, interventricular septum thickness （IVSd）, left ventricle posterior wall thickness （LVPW）, right ventricular dimension （RVD）, left atrium （LA） and ejection fraction （EF）.RESULTS： A total of 146 patients with stage 1 to 5 CKD were enrolled. Serum hepcidin-25 levels were 16.51 ± 5.2, 17.59 ± 5.32, 17.38 ± 6.47, 19.98 ± 4.98 and 22.03 ± 4.8 ng/mL for stage 1 to 5 CKD patients, respectively. Hepcidin-25 level was independently pre-dicted by the serum ferritin level （β = 0.6, P = 0.002） and the estimated glomerular fltration rate （β = -0.48, P = 0.04）. There were negative correlations between the serum hepcidin level and the LVM and LVMI （ P = 0.04 and P = 0.005, respectively）. Systolic blood pressure （BP） was positively correlated with the LVMI （ P = 0.005）. In the multivariate analysis, a decreased serum hepci-din-25 level was independently associated with a higher LVMI （β = -0.28, 95%CI： -0.48 - -0.02, P = 0.006） after adjusting for body mass index, age and systolic BP.CONCLUSION： A lower serum hepcidin level is associ-ated with a higher LVMI in CKD patients. Low hepcidin levels may be independently correlated with unfavor-able cardiovascular outcomes in this population.展开更多
AIM:To investigate hepcidin expression,interleukin-6(IL-6)production and iron levels in the rat colon in the presence of trinitrobenzene sulfonic acid(TNBS)-induced colitis.METHODS:In rats,we evaluated the severity of...AIM:To investigate hepcidin expression,interleukin-6(IL-6)production and iron levels in the rat colon in the presence of trinitrobenzene sulfonic acid(TNBS)-induced colitis.METHODS:In rats,we evaluated the severity of colitis induced by repeated TNBS administration using macroscopic and microscopic scoring systems and myeloperoxidase activity measurements.The colonic levels of hepcidin,tumor necrosis factor alpha(TNF-α),IL-10 and IL-6 were measured by Enzyme-Linked Immunosorbent Assay,and hepcidin-25 expression and iron deposition were analyzed by immunohistochemistry and the Prussian blue reaction,respectively.Stat-3 phosphorylation was assessed by Western blot analysis.Hematological parameters,iron and transferrin levels,and transferrin saturation were also measured.Additionally,the ability of iron,pathogen-derived molecules and IL-6 to induce hepcidin expression in HT-29 cells was evaluated.RESULTS:Repeated TNBS administration to rats resulted in macroscopically and microscopically detectable colon lesions and elevated colonic myeloperoxidase activity.Hepcidin-25 protein levels were increased in colonic surface epithelia in colitic rats(10.2±4.0pg/mg protein vs 71.0±8.4 pg/mg protein,P<0.01).Elevated IL-6 levels(8.2±1.7 pg/mg protein vs 14.7±0.7 pg/mg protein,P<0.05),TNF-αlevels(1.8±1.2pg/mg protein vs 7.4±2.1 pg/mg protein,P<0.05)and Stat-3 phosphorylation were also observed.Systemic alterations in iron homeostasis,hepcidin levels and anemia were not detected in colitic rats.Iron deposition in the colon was only observed during colitis.Hepcidin gene expression was increased in HT-29 cells after IL-6 and lipopolysaccharide[a toll-like receptor 4(TLR-4)ligand]treatment.Deferoxamine,ferric citrate and peptidoglycan(a TLR-2 ligand)were unable to alter the in vitro expression of hepcidin in HT-29 cells.CONCLUSION:Colitis increased local hepcidin-25 expression,which was associated with the IL-6/Stat-3 signaling pathway.An increase in local iron sequestration was also observed,but additional studies are needed to determine whether this sequestration is a defensive or pathological response to intestinal inflammation.展开更多
基金Grants from the Department of Health(DOH 97-HP-1103)
文摘AIM： To assess the correlation between the serum hep-cidin-25 level and left ventricular mass index.METHODS： This study was a cross-sectional study conducted between March 2009 and April 2010. Demo-graphic and biochemical data, including the serum hep-cidin-25 level, were collected for chronic kidney disease （CKD） patients. Two-dimensional echocardiography was performed to determine the left ventricle mass （LVM）, left ventricular mass index （LVMI）, interventricular septum thickness （IVSd）, left ventricle posterior wall thickness （LVPW）, right ventricular dimension （RVD）, left atrium （LA） and ejection fraction （EF）.RESULTS： A total of 146 patients with stage 1 to 5 CKD were enrolled. Serum hepcidin-25 levels were 16.51 ± 5.2, 17.59 ± 5.32, 17.38 ± 6.47, 19.98 ± 4.98 and 22.03 ± 4.8 ng/mL for stage 1 to 5 CKD patients, respectively. Hepcidin-25 level was independently pre-dicted by the serum ferritin level （β = 0.6, P = 0.002） and the estimated glomerular fltration rate （β = -0.48, P = 0.04）. There were negative correlations between the serum hepcidin level and the LVM and LVMI （ P = 0.04 and P = 0.005, respectively）. Systolic blood pressure （BP） was positively correlated with the LVMI （ P = 0.005）. In the multivariate analysis, a decreased serum hepci-din-25 level was independently associated with a higher LVMI （β = -0.28, 95%CI： -0.48 - -0.02, P = 0.006） after adjusting for body mass index, age and systolic BP.CONCLUSION： A lower serum hepcidin level is associ-ated with a higher LVMI in CKD patients. Low hepcidin levels may be independently correlated with unfavor-able cardiovascular outcomes in this population.
基金The Fundacao de Amparo a Pesquisa do Estado de Sao Paulo,No. FAPESP 2010/02991-6
文摘AIM:To investigate hepcidin expression,interleukin-6(IL-6)production and iron levels in the rat colon in the presence of trinitrobenzene sulfonic acid(TNBS)-induced colitis.METHODS:In rats,we evaluated the severity of colitis induced by repeated TNBS administration using macroscopic and microscopic scoring systems and myeloperoxidase activity measurements.The colonic levels of hepcidin,tumor necrosis factor alpha(TNF-α),IL-10 and IL-6 were measured by Enzyme-Linked Immunosorbent Assay,and hepcidin-25 expression and iron deposition were analyzed by immunohistochemistry and the Prussian blue reaction,respectively.Stat-3 phosphorylation was assessed by Western blot analysis.Hematological parameters,iron and transferrin levels,and transferrin saturation were also measured.Additionally,the ability of iron,pathogen-derived molecules and IL-6 to induce hepcidin expression in HT-29 cells was evaluated.RESULTS:Repeated TNBS administration to rats resulted in macroscopically and microscopically detectable colon lesions and elevated colonic myeloperoxidase activity.Hepcidin-25 protein levels were increased in colonic surface epithelia in colitic rats(10.2±4.0pg/mg protein vs 71.0±8.4 pg/mg protein,P<0.01).Elevated IL-6 levels(8.2±1.7 pg/mg protein vs 14.7±0.7 pg/mg protein,P<0.05),TNF-αlevels(1.8±1.2pg/mg protein vs 7.4±2.1 pg/mg protein,P<0.05)and Stat-3 phosphorylation were also observed.Systemic alterations in iron homeostasis,hepcidin levels and anemia were not detected in colitic rats.Iron deposition in the colon was only observed during colitis.Hepcidin gene expression was increased in HT-29 cells after IL-6 and lipopolysaccharide[a toll-like receptor 4(TLR-4)ligand]treatment.Deferoxamine,ferric citrate and peptidoglycan(a TLR-2 ligand)were unable to alter the in vitro expression of hepcidin in HT-29 cells.CONCLUSION:Colitis increased local hepcidin-25 expression,which was associated with the IL-6/Stat-3 signaling pathway.An increase in local iron sequestration was also observed,but additional studies are needed to determine whether this sequestration is a defensive or pathological response to intestinal inflammation.
