Protective effect and mechanism of hepcidin in rats with alcoholic liver damage / 中华肝脏病杂志

<p><b>OBJECTIVE</b>To study the mechanism of how iron-regulatory protein (hepcidin) affect iron overload in alcoholic liver disease (ALD).</p><p><b>METHODS</b>Thirty male wistar rats were randomly divided into 3 groups: Lieber-Decarli liquid without alcohol group (control group), Lieber-Decarli liquid with alcohol (alcohol group) and hepcidin intraperitoneally injected group (hepcidin group), each rat was fed for 6 weeks. The Serum concentration of Alanine Aminotransferase (ALT), Aspartate Amino Transferase (AST), Iron, Total Iron Binding capacity (TIBC), Ferritin, Malonyl Dialdehyde (MDA) and Hepcidin were determined. Hepatic tissue was examined by hematoxylin and eosin staining, prussian blue iron staining and immunohistochemistry staining.</p><p><b>RESULTS</b>(1) Serum concentration of ALT in control group, alcohol group and hepcidin group were (25.2 ± 4.6) U/L, (37.9 ± 14.3) U/L and (40.9 ± 14.1) U/L (F = 4.907, P < 0.05), respectively. Serum AST among three groups were (32.3 ± 13.4) U/L, (55.0 ± 18.6) U/L and (48.3 ± 26.0) U/L (F = 3.742, P < 0.05), respectively. The secretions of ferritin were (224.72 ± 85.49) ng/ml, (345.59 ± 124.75) ng/ml and (339.47 ± 138.47) ng/ml (F = 3.539, P < 0.05). The serum concentrations of TIBC were (147.30 ± 31.98) μmol/L, (148.04 ± 58.74) μmol/L and (143.28 ± 37.38) μmol/L (F = 1.209, P > 0.05), respectively. The serum concentrations of iron were (55.64 ± 13.32) μmol/L, (60.37 ± 25.89) μmol/L and (49.77 ± 17.64) μmol/L (F = 0.651, P > 0.05), respectively. The serum concentration of MDA were (5.84 ± 2.17) nmol/ml, (6.51 ± 2.23) nmol/ml and (4.27 ± 2.68) nmol/ml (F = 2.782, P > 0.05), respectively. The serum concentration of Hepcidin were (155.96 ± 44.91)ng/ml, (124.11 ± 31.98) ng/ml and (114.96 ± 25.81) ng/ml (F = 3.839, P < 0.05), respectively. (2) Significant fat change observed in the liver of alcohol group. The positive granulations of iron staining were (0.8 ± 1.0), (1.2 ± 1.6) and (1.1 ± 1.1) (F = 0.254, P > 0.05), respectively. No differences found of liver iron express among the three groups. Intraperitoneal injection of hepcidin increased hepcidin expression in liver which was inhibited by alcohol (F = 4.139, P < 0.05).</p><p><b>CONCLUSIONS</b>ALD rats with lower hepcidin expression in liver can result in iron metabolism disorder. Ectogenic hepcidin can protect liver against alcohol damage by inhibiting lipid peroxidation.</p>

Analysis of translocation of the CagA protein and induction of a scattering phenotype in AGS cells infected with Helicobacter pylori / 生物医学与环境科学（英文）

<p><b>OBJECTIVE</b>To investigate whether the presence of structured CagA proteins in Western- and Eastern-type Helicobacter pylori (H. pylori) induces different incidences of gastric diseases.</p><p><b>METHODS</b>CagA and phosphorylated CagA were expressed in AGS gastric epithelial cells infected with wild type and mutant strains. The ability of individual CagA was determined by immunoprecipitation and Western blot assay. Morphological changes of these cells were observed under microscope to evaluate the appearance of elongation hummingbird phenotype.</p><p><b>RESULTS</b>The sizes of CagA proteins in different strains were different, and no phosphorylated CagA proteins were detected in wild-type strains. Meanwhile, the kinetics of CagA status in AGS infected with H. pylori was detected. The molecular weight of phosphorylated CagA with the same size of CagA proteins in H. pylori was different in infections with different wild-type strains. CagA and phosphorylated CagA increased in a time-dependent manner after the infection. The hummingbird phenotype with H. pylori for time-course was observed under microscope. Instead of HPK5 strain, the wild-type 26695 strain induced hummingbird phenotype in a time-dependent manner.</p><p><b>CONCLUSION</b>Translocation and phosphorylation of CagA are necessary, but not sufficient, for the induction of hummingbird phenotype in AGS cells.</p>

Study on the association of the CRP gene +1444C/T polymorphism with symptomatic carotid artery stenosis / 中华医学遗传学杂志

<p><b>OBJECTIVE</b>To investigate the potential association of the C-reactive protein (CRP) gene +1444C/T polymorphism with symptomatic carotid artery stenosis.</p><p><b>METHODS</b>Polymerase chain reaction-restriction fragment length polymorphism was used for the detection of CRP +1444C/T genotypes in 192 patients with symptomatic carotid artery stenosis and 197 healthy controls. Serum high sensitivity-CRP (hs-CRP) levels were measured by routine method.</p><p><b>RESULTS</b>No TT genotype was detected in this study. Patients with >70% stenosis had higher CC genotype compared with those with <70% stenosis after adjusting for major cerebrovascular risk factors (OR: 2.958; 95% CI: 1.198 - 7.305; P=0.019). CRP levels were significantly higher in patients than in controls. Subgroup analysis according to clinical characteristics (single or double stenosis; >70% or <70% stenosis) did not show difference in CRP levels. There was no significant difference in the prevalence of CT genotype between patients and controls, or between single and double stenosis (P>0.05).</p><p><b>CONCLUSION</b>The CRP +1444 CC genotype is a risk factor for >70% carotid artery stenosis. The serum CRP level is associated with the presence of carotid stenosis. However, it is not associated with the number and severity of stenosis.</p>