AIM:To study the effect of chronic corticosterone ( CORT) injection on the depression-like behav-iors and the brain glycogen level in mice.METHODS:Male C57BL/6N mice (n=40) were randomly divided into nor-mal control group and model group.The mice in model group were subcutaneously consecutively injected with CORT for 4 weeks.The mouse model of chronic stress depression was constructed.The forced swim test and open field experiment were conducted to prove chronic stress model.The serum level of CORT in the mice was measured by radioimmunoassay.The protein levels of hippocampal synaptophysin ( SYP) and brain-derived neurotrophic factor ( BDNF) were detected by West-ern blot.Hippocampus glycogen, glycogen synthase and glycogen phosphorylase were determined by indirect fluorescence measurement.RESULTS:Compared with normal control group, the immobility time of the forced swim test in model group was significantly lengthened (P<0.01), and the ability of spontaneous activity was reduced (P<0.01), indicating that chronic CORT injection induced depression-like behaviors in mice.The CORT level increased significantly (P<0.01) in model group.CORT injection decreased the protein expression of hippocampal SYP and BDNF (P<0.01), reduced hipp-ocampal glycogen level (P<0.05) and glycogen synthase activity (P<0.05), and increased glycogen phosphorylase ac-tivity (P<0.05).CONCLUSION:Chronic CORT injection causes hippocampal neuron damage and induces the depres-sion-like behaviors of mice, which may be associated with decreasing hippocampal glycogen level by CORT.

Objective To study the effects of long-term injection of corticosterone (CORT) on the hippocampal astrocytes and synaptic plasticity in mice.Methods Male C57BL/6N mice (n=40) were randomly divided into control group and model group.Mice in the model group were treated with subcutaneous injection of CORT for 4 weeks to generate chronic stress depression model.Chronic stress model was proved to be established by tail suspension test and sucrose preference test and serum level of CORT was determined by radioimmunoassay.Protein expression levels of hippocampal synaptophysin (SYP) and postsynaptic density-95 (PSD-95) were detected by Western blot.Somal volume and protrusion length of glial fibrillary acidic protein-positive astrocytes were assayed by immunocytochemistry and quantitative stereological techniques.Results Immobility time in model group ((137.95±6.22) s) was significantly extended in comparison with that in the control group ((114.05 ± 4.12) s) (P＜ 0.01).Sucrose preference in the model group (62.42 ± 6.75)％ was lower than that in the control group (86.52±5.08)％ (P＜0.01).CORT levels in model group ((11.48±0.62) ng/ml) was significantly increased compared with that in the control group ((1.11±0.05) ng/ml) (P＜0.01).Hippocampal SYP (0.54±0.04) and PSD-95 (0.57±0.07) expression levels in model group were lower than those in the control group (0.99±0.14),(1.03±0.10) (P＜0.01).Somal volume in the model group ((132.04±9.23) μm3) and protrusion length ((1.39± 0.05) × 107 μm) was lower than that in the control group ((168.49±9.01)μm3),(1.77±0.10) × 107 μm) (P＜0.05,P＜0.01).SYP and PSD-95 expression level was found to be positively correlated with the reduction of the protrusion length(r=0.660,P＜0.01;r=0.614,P＜0.01)in astrocytes.Conclusion The results suggest that depression-like behavior-in-duced by long-term CORT treatment is possibly caused by the alternation of the synaptic plasticity associated with the reduction of the reducing the protrusion length.

Background The incidence of primary open angle glaucoma (POAG) is increasing in recent years.To study the risk factors of POAG pathogenesis is of great significance.Objective This study was to explore the association between Helicobacter pylori infection and POAG pathogenesis.Metbods The Chinese and English literature about Helicobacter pylori infection and pathogenesis from January 2000 to February 2015 was searched in PubMed,Embase,The Cochrane Library,VIP,Wanfang database and CNKI database with computer and supplemented by the relevant references,and these cases-control studies were evaluated using the Newcastle-Ottawa Scale (NOS).The odds ratio (OR) and 95％ confidence interval (CI) were calculated by using Stata 12.0 statistical software.Sensitivity analysis and subgroup analysis were used to process the heterogeneity (I2) among the studies.The effect size was analyzed using the randomized model in I2 ≥50％ and fixed model was used in I2＜50％.Results Eight cases-control studies from Erope,Asia and North America were included with the NOS scores ≥ 5.The examination methods for Helicobacter pylori included ELISA,Western blot and histopathology among the articles.Helicobacter pylori infection rate was 71.38％ (197/276) in the POAG group,and that in the control group was 42.90％ (151/352).Randomized model analysis showed a significant association between Helicobacter pylori infection and POAG pathogenesis (OR =3.23,95％ CI:1.65-6.23,P =0.001).No obvious interference from any paper was found by sensitivity analysis.The subgroup analysis based on different areas found that Helicobacter pylori infectious rate of POAG patients was highest in Europe area (OR =7.25,95 ％ CI:3.61-14.54,P =0.000,I2 =0.0％),the subgroup based on different detect methods found that histopathological examination had the highest detected rate of Helicobacter pylori (OR=9.13,95％ CI:3.78-22.04,P=0.000,I2 =0.0％),and the next was ELISA assay (OR=2.85,95％ CI:1.40-5.81,P =0.004,I2 =60.4％).No published bias was seen by funnel plots and Egger linear analysis.Conclusions Helicobacter pylori infection is associated with POAG pathogenesis.

ObjectiveTo investigate the risk factors of early rebleeding after ruptured intracranial aneurysm embolization surgery.MethodsForty-two patients with early postoperative rebleeding after ruptured intracranial aneurysm embolization surgery(study group) were enrolled,and 40 patients without early postoperative rebleeding after ruptured intracranial aneurysm embolization surgery at the same period was selected randomly as control group.Single factor and multiple factors were analyzed by non-condition Logistic regression model.ResultsThe single factor analysis result showed that age ≥50,history of hypertension,diabetes history,ruptured frequency number ≥2,combined with vasospasm,postoperative anticoagulation therapy,postoperative blood pressure fluctuation ≥ 30 mm Hg (1 mm Hg =0.133 kPa),pseudoaneurysm,fatal embolism and most embolism in study group [81.0％(34/42),76.2％(32/42),66.7％(28/42),76.2％ (32/42),81.0％ (34/42),76.2％ (32/42),66.7％ (28/42),66.7％ (28/42),66.7％ (28/42) ]had statistical differences compared with those in control group [57.5％ (23/40),50.0％ (20/40),37.5％( 15/40 ),50.0％ ( 20/40 ),57.5％ ( 23/40 ),47.5％ ( 19/40 ),37.5％ ( 15/40 ),37.5％ (15/40),37.5％ ( 15/40) ](P ＜0.05).Further multiple factors analysis showed that age ≥50,history of hypertension,ruptured frequency number ≥ 2,combined with vasospasm,postoperative anticoagulation therapy,postoperative blood pressure fluctuation ≥ 30 mm Hg were the independent risk factors of early postoperative rebleeding after ruptured intracranial aneurysm embolization surgery (P ＜0.05).ConclusionsAge ≥50,history of hypertension,ruptured frequency number ≥ 2,combined with vasospasm,postoperative anticoagulation therapy,postoperative blood pressure fluctuation ≥ 30 mm Hg are the independent risk factors of early postoperative rebleeding after ruptured intracranial aneurysm embolization surgery.The necessary interventions to these risk factors have important significance,and can lower the incidence of early postoperative ruptured rebleeding after ruptured intracranial aneurysm embolization surgery and improve the prognosis.

Animals ; Free Radical Scavengers ; pharmacology ; Hyperlipidemias ; blood ; Hypolipidemic Agents ; pharmacology ; Lipids ; blood ; Male ; Peptides ; pharmacology ; Rats ; Rats, Sprague-Dawley ; Superoxide Dismutase ; blood

AIM:To investigate the effects of grape polyphenol ( GP) on caerulein-induced acute pancreatitis (AP) in mice.METHODS:Two-month-old female mice of ICR strains (n=21) were randomly divided into 3 groups:normal control ( NC) group, AP group, and GP-treated AP group.Before AP induction, the mice in GP-treated AP group were continuously administrated with 1.5 g/kg GP aqueous solution by gavage for 7 d, while those in NC group and AP group were treated with saline as a vehicle control.On the 7th day, the mice in AP group and GP-treated AP group were in-traperitoneally injected with caerulein (50μg/kg) in 1 h interval for 7 serial injections in total.The mice in NC group were treated with saline according to the same procedure in experimental group.All the mice were sacrificed 24 h after AP induc-tion, and the pancreatic tissues and lung tissues were harvested for further investigation of the pathological changes, macro-phages infiltration, myeloperoxidase ( MPO ) activity and expression of inflammatory and oxidative stress factors.RE-SULTS:Compared with AP group, the mice in GP-treated AP group showed milder morphological changes and lower path-ological scores, including the scores of edema, inflammation and vacuolization (P<0.05), but the necrosis scores and to-tal scores showed no statistical difference between these 2 groups.Besides, the mice in GP-treated AP group had fewer macrophage infiltration, lower lung MPO activity (P<0.01), and lower expression of inflammatory factors, tumor necrosis factor α(TNF-α)and monocyte chemotactic protein 1 (MCP-1) (P<0.05), and oxidative stress factors, superoxide dis-mutase (SOD)-1, SOD-2 and NADPH oxidase 2 (NOX-2) (P<0.01).CONCLUSION:Grape polyphenol has remark-able protective effect on pancreatic tissues of mice with caerulein-induced acute pancreatitis, and the mechanisms may be related to down-regulation of inflammatory and oxidative stress factors.

Objective To detect the express of the pulmonary fibrosis factor CTGF,TGF-β1 and the senescence correlated β-Gal in the primary pulmonary bulla,and investigate the correlation of the pulmonary fibrosis factor,cell senescence and the development of the primary pulmonary bulla.Methods The expression of CTGF,TGF-β1 and β-Gal protein in the tissue of normal lung tissues and lung bullae were tested.The cell image extracted with the digital camera system was entered into the Image-pro Plus 6.0 morphology Image analysis system and analyzed with Semi-quantitative way.Results The expression level of TGF-β1 and CTGF in primary pulmonary bulla organization was obviously higher than that of normal lung tissue.There was a statistically significant difference(P ＜ 0.05).CTGF and TGF-β1 expression level had a significant correlation (r =0.965,P ＜ 0.01).β-Gal expression level of primary pulmonary bullae had no obvious difference with normal lung tissue.Conclusion CTGF and TGF-β1 may play an important role in the formation of primary pulmonary bulla.Both play a synergistic role in the formation of primary pulmonary bulla.Cell senescence is not relevanted with the formation of primary pulmonary bulla.

Objective To establish an eukaryotic vector of monkey B virus glycoprotein D gene and analyze the expression of gD gene in human embryonic kidney 293T cells.Method First, the protein of monkey B virus glycoprotein D was obtained by gene synthesis.The gene fragments were digested with Pst I and Not I, and ligated to pEGPF-N3. Then, the recombinant plasmid pEGPF-N3-GD was transfected into 293T cells.The expression of gD protein in the cells was detected by Western blot, and the expression localization was investigated using laser scanning confocal microscopy. Results The recombinant plasmid pEGPF-N3 carrying gD gene was successfully constructed, and normally expressed in the 293T cells.Conclusions Glycoprotein D of monkey B virus is expressed successfully in the 293T cells and the protein is located on the cell surface.It may be useful for the preparation of specific recombinant antigen to the glycoprotein D of monkey B virus on cell surface, and can be also used for preparation of antigen slide for detection of monkey B virus.

Objective: To investigate the combined preventive effect of folic acid (FA) and vitamin B12 (VB12) on the developmental toxicity of alcohol. Methods: To build animal model with the developmental toxicity by giving 5g/kg bw alcohol (25% ethanol) intragastrically (IG) to ICR mice during gestational day (GD) 6-15. In addition to alcohol, three groups were given FA 60 mg/kg bw, VB12 1 mg/kg bw, FA 60 mg/kg bw + VB12 1 mg/kg bw respectively by IG during GD1-GD16. An alcohol model group and a negative control group were set. All dams were killed at GD18. Results: Compared to the alcohol model group, the pregnant mice of FA + VB12 combined intervention group put on more weight during pregnancy; the live fetal rate; the fetal weight, body length and tail length were all increased; the abnormal ossification rate of sternum, occipital bone, and four limbs dropped (P

AIM To explore pharmacokinetics of Berberine in YL2000 in normal and febrile rats. METHODS The levels of Berberine in plasma were measured through HPLC and secondary parameters were obtained by fitting the dose time data of Berberine making use of 3P87 programme. RESULTS In normal and febrile rats, the plasma concentration of Berberine was peaked at (3 4?0 3) h vs (0 3?2 1) h( P