AIM: To study the role of p38 mitogen-activated protein kinase (p38MAPK) activation in high glucose-induced collagen Ⅲ synthesis in NRK52E cells. METHODS: Normal rat tubular epithelial cell line NRK52E was cultured in D-glucose of different concentrations, pretreated with SB203580 and collected at different time points. The levels of phospho-p38MAPK and extracellular matrix collagen Ⅲ were examined by Western blotting. RESULTS: The activation of p38MAPK was shown to be dependent upon D-glucose concentration and the time-course. Pretreatment with SB203580 blocked p38MAPK activation induced by high concentration of D-glucose in NRK52E cells. CONCLUSIONS: The activation of p38MAPK induced by high concentration of glucose may play a role in diabetic interstital renal fibrosis. SB203580 has a potential value of clinical applications in the prevention and treatment of diabetic nephropathy.

Objective To explore the relationships between the expression of PECAM-1 and the degree of ALI in Paraquat induced lung injury model of rabbits. Method Thirty six adult New Zealand rabbits were randomly divided into three groups: 8 mg/kg (Group A), 16 mg/kg (Group B) and 32 mg/kg ( Group C) according to the dose of Paraquat which were infusion into stomach. After poisoned, the animals were monitored for seven days, and then sacrificed. The upper lobe of lung were removed for HE,Masson staining and immunohistochemisty. The ALl score, fibrosis of lung and expression of PECAM-1 were semiquantitative analyzed. Results Each group has 12 animals suffered from poisoning. The survival time of animals in Group C was (6. 47 ± 0. 99 ) days, shorter than (6. 09 + 1.04) days ( P = 0. 031 ) in Group B and (4. 77 + 2. 04) days ( P = 0. 0 07) in Group A. The ALI score were ( 8. 33 ± 1.03) points in Group A, superior to (9. 83 ± 1.17) points ( P = 0. 047 ) in Group B and ( 11.50 + 1.38) points ( P ＜ 0. 01 ) in group C, Group B vs Group C, P=-0.03o The fibrosis degree of lung was (31.09 +2.05)% in Group A,not severe as (34. 37 ±1.62)% (P=0. 002) in Group B and (36. 54 ±0. 44)% (P ＜0. 01 ) in Group C, Group B vs Group C, P = 0. 026. The Pearson correlation analysis showed the expression of PECAM-1 was negative correlated to ALI score (Coe = -0. 732, P =0. 001 ) and fibrosis degree of lung (Coe = -0. 779, P ＜ 0. 001 ) . Conclusions The expressions of PECAM-1 were significantly decreased in New Zealand after Paraquat poisoned, which were dose dependent, correlated to ALI scored and fibrosis degree of lung, so it may play an important role in the development of lung injured induced by Paraquat.

Objective To investigate the incidence of systemic inflammatory response syndrome(SIRS) after cardiopulmonary resuscitation(CPR) and to observe the effect of Ulinastain in inhibition of inflammatory mediator.Methods Forty patients surviving more than 48 hours after CPR were divided into Ulinastain and control groups randomly. Activity of nuclear factor kappa B(NF-?B), IL-6,TNF-? of the patients was detected .All patients were evaluated by SIRS diagnosis standard and their general organ function was examined. All data were compared between two groups.Results Activities of NF-?B, IL-6,TNF-? of patients after CPR was significantly higher than that of normal people (P

AIM:To observe the characterization in neural cells derived from the hippocampus of embryonic rats and to examine the effect of myelin-associated glycoprotein(MAG) on the proliferation,differentiation and neurite growth of neural stem cells(NSCs).METHODS:The hippocampus cells of embryonic rats were isolated and cultured in vitro.The expressions of nestin and doublecortin,the marks of NSCs,were observed by immunocytochemical method.The rate of proliferating cells was examined by BrdU immunocytochemistry.The average neuronal neurite length and the percentage of differentiated neurons were detected by immunocytochemistry staining.RESULTS:The hippocampus cells of 16 days old embryonic rats had the characteristics of NSCs.The percentage of differentiated neurons(?-tubulin Ⅲ-positive cells) was 18.17%?2.79% and the average neuronal neurite length was(136.27?33.66)?m,seven days after the differentiation initiated in vitro in control group.After NSCs were treated with MAG-Fc(200 ?g/L),the percentage of differentiated neurons and the average neurite length were decreased,respectively,to 10.05%?3.42%(P0.05).CONCLUSION:MAG-Fc inhibits the differentiation and neurite growth of the NSCs,but has no effect on the proliferation.

Objective To explore the effects of estrogen on oxidative stress of the lung tissue induced by acute paraquat (PQ) poisoning. Methods Thirty-two male adult New Zealand rabbits were randomly divided into model group and estrogen intervention group, 16 rabbits in each group. The model of lung injury induced by PQ poisoning was reproduced by feeding 16 mg/kg of 20% PQ through gastric tube. The rabbits in estrogen intervention group received intravenous infusion of 5 mg/kg estrogen after PQ challenge for 7 days, and the rabbits in model group received an equal volume of normal saline. Three rabbits in each group were sacrificed at 1, 2 and 3 days respectively after exposure. The lung tissue was harvested, the levels of reactive oxygen species (ROS) was determined by 2',7'-dichlorofluorescin diacetate (DCFH-DA), malondialdehyde (MDA) was determined by thiobarbituric acid (TBA), the mRNA expression of manganese-containing superoxide dismutase (MnSOD) was determined by reverse transcription-polymerase chain reaction (RT-PCR), and adenosine triphosphatase (ATP) content in mitochondrion was determined by enzyme linked immunosorbent assay (ELISA). The pathological changes in lung were observed under light microscopy using hematoxylin and eosin (HE) staining, and the lung injury was evaluated with lung injury score. Results The contents of ROS and MDA in lung within 3 days after PQ poisoning were gradually increased, and MnSOD mRNA expression and ATP content were gradually decreased. Estrogen intervention could significantly reduce the production of ROS and MDA after PQ poisoning [3-day ROS (fluorescence intensity): 161.05±30.04 vs. 188.30±31.80, 3-day MDA (mmol/L): 98.71±0.92 vs. 122.12±1.24], up-regulate MnSOD mRNA expression (integral A value: 3.05±0.90 vs. 1.22±0.24), and increase ATP content in mitochondrion (ng/L: 3.75±0.92 vs. 2.28±0.29) with statistically significant differences (all P < 0.01). In lung tissue after PQ poisoning, congestion, edema, focal pulmonary consolidation, pulmonary interstitial and alveolar space were infiltrated by a large number of neutrophil, alveolar interval were thickened obviously and the above phenomenon were most serious at 3 days after poisoning as shown under optical microscope. Estrogen intervention could significantly improve lung injury as compared with that of model group, and the lung injury score at 3 days was significantly lower than that of model group (11.8±0.7 vs. 13.5±1.0, P < 0.01). Conclusions The oxidative stress indicators in the lung tissue after PQ poisoning were obviously abnormal, the pathological damage was serious with time dependence. The administration of estrogen can reduce acute lung injury after PQ poisoning by reducing the oxidative stress.

Objective To determine the levels of soluble thrombomodulin(sTM) in patients with acute pulmonary embolism (PE), and evaluate sTM clinical significance.Methods The sTM levels were determined with enzyme linked immunosorbent assay in PE patients, and compared with healthy control group. Eighteen PE patients were divided into massive PE group and non - massive PE group, non - respiratory failure group and respiratory failure group, and compared the sTM level in the groups. Results Level of sTM in PE patients was higher than that of control group (P

[Objective] To investigate the inhibitory effect of CTLA-4Ig fusion protein on atherosclerosis in the mice with an apolipoprotein-E gene defect fed on cholesterol diet.[Methods] Twenty-five male 10-week-old ApoE-/- mice were selected and fed on cholesterol diet for 4 weeks,5 out of which were executed at random as control group and their pathological sections were kept to observe the early fatty streaks.The other 20,divided into CTLA-4Ig treatment group,PBS group,IgG1 group,and blank group at random,5 in each.Three groups were given intraperitoneal injection of CTLA-4Ig (10 μg per time),PBS (100 μL per time),Rat-IgG1 (10 μg per time) respectively,twice a week,for 8 weeks.The blank group has no treatment.Followed by 8-week treatment,the whole aorta from the root to crotch of iliac artery was separated after anesthesia with the intraperitoneal injection of 1 % pentobarbital.Subsequently,the area ratio of plaque and lumen,the thickness ratio of endangium and tunica media,the lipid-soaking extent intra-plaque and the content of collagen fibrils and smooth muscle cells intra-plaque were analyzed by image-processing soft.[Results] After fed on cholesterol diet for 4 weeks,there were obviously atherosclerosis in the aorta in the ApoE-/- mice.There were typical atherosclerotic plaque in ApoE-/- mice fed on cholesterol diet after another 8 weeks.The area ratios of plaque and lumen in CTLA-4Ig group,PBS group,IgG1 group,and blank group were 0.27 ± 0.08,0.40 ± 0.08,0.43 ± 0.08,and 0.46 ± 0.10,and obviously increased than those in control group (0.05 ± 0.01,P ＜ 0.05).The thickness ratios of endangium and tunica media in four groups were 2.6 ± 0.6,6.0 ± 0.9,5.7 ± 0.8,and 5.9 ± 0.6 and obviously increased than those in control group (0.5 ± 0.1,P ＜ 0.05).The lipid-soaking extent intra-plaque in experimental groups were 26.0 ± 3.0,40.8 ± 5.7,40.6 ± 3.0,and 43.2 ± 5.7,and were obviously increased than those in control group (7.2 ± 1.4,P ＜ 0.05 ).It was found that the area ratio of plaque and lumen,the thickness ratio of endangium and tunica media,and the lipid-soaking extent intra-plaque in CTLA-4Ig group were significantly lower than those in PBS group,IgG1 group,and blank group (P ＜ 0.05),but there was no significant difference in those between the PBS group,IgG1 group,and blank group (P ＞ 0.05).The content of collagen fibrils in CTLA-4Ig group were 16.0 ± 1.1 and higher than those in PBS group,IgG1 group,and blank group (8.6 ± 1.2,9.2 ± 1.5,and 9.0 ± 1.3,P ＜ 0.05).The content of smooth muscle cells in plaque in CTLA-4Ig group were 11.8 ± 1.0 and higher than those in PBS group,IgG1 group,and blank group (7.8 ± 0.8,7.5 ± 0.9,and 7.3 ± 0.7,P ＜ 0.05).There was no significant difference in content of collagen fibrils and smooth muscle cells between the PBS group,IgG1 group,and blank group (all P ＞ 0.05).[Conclusion] CTLA-4Ig fusion protein could evidently inhibit the atherosclerosis progression and enhance the stability of plaque through increasing the content of collagen fibrils produced by smooth muscle cells intra-plaque in ApoE-/- mice fed on cholesterol diet.

Objective To evaluate the effect of percutaneous coronary intervention (PCI) or thrombolysis,in patients with return of spontaneous circulation (ROSC) after out-of-hospital cardiac arrest (OHCA),in the presence of ST-elevation myocardial infarction (STEMI).We demonstrated the benefits of the two therapies on ROSC patients in hospital discharge and neurological recovery,and clarified the importance of ROSC,so as to guide the treatments for OHCA in the presence of STEMI.Methods It was performed a meta-analysis of clinical studies located in PUBMED and MEDLINE databases from January 1995 to October 2011.OHCA patients with ROSC were as our study objects,the hospital discharge and neurological recovery rates,of patients with and without PCI or thrombolysis,were assessed in patients with ROSC after OHCA in the presence of STEMI.In the same Cohort Study,between received and rejected PCI,or between received and rejected thrombolysis in OHCA patients with ROSC as treated group and control group,using Review Manager 5.1 software to analyze,respectively.Furthermore,we also compared the differences in hospital discharge and neurological recovery rates between patient groups who received PCI or thrombolysis by Pearson x2 analysis.Results The meta-analysis showed that the rate of hospital discharge improved with both PCI (odds ratio [OR],1.65 ; 95％ confidence interval [CI],1.05-2.59,P ＜ 0.01)and thrombolysis (OR,2.03 ; 95％ CI,1.24-3.34,P ＜ 0.01) in patients with ROSC after OHCA,in the presence of STEMI.We also found that there were not significant differences between with PCI and with thrombolysis in the rate of hospital discharge (63.00％ vs.65.19％,P =0.548) and neurological recovery (88.62％ vs.91.25％,P =0.351) for the patients with ROSC after OHCA (P ＞0.05).Conclusions In patients with ROSC after OHCA in the presence of STEMI,both PCI and thrombolysis improved hospital discharge rates.Furthermore,there were similar efficacy in hospital discharge and neurological recovery rates between with PCI and with thrombolysis.

Objective To detect the level of plasma microRNA-1 (miR-1) in acute myocardial infarction (AMI) and compare the diagnostic values of it with that of cardiac troponin T (cTnT).Methods During 2011-05 to 2012-05,there were fifty-six plasma samples taken from patients with AMI and twenty-eight plasma specimens got from non-AMI controls were analyzed.The expression of plasma miR-1 was measured by quantitative reverse transcription-polymerase chain reaction (qRT-PCR),and the level of plasma cTnT was measured by using electrochemiluminescence-based methods on the Elecsys 2010 Immunoassay Analyzer.Then,the SPSS 16.0 was used for the statistical analysis.Data were presented as means ± standard deviation unless otherwise described.The differences about clinical characteristics between AMI patients and controls were tested using Student' s t-test or Fisher' s exact test.The Mann-Whitney test was conducted to compare the expression of microRNAs between the AMI patients and controls.The comparison of microRNAs expression between different intervals of AMI patients was done using Wilcoxon signed rank test.The receiver operating characteristic (ROC) curve was established to discriminate AMI patients from controls.Results The expression of plasma miR-1 was significantly increased in AMI patients (P ＜ 0.01) compared with healthy controls.The contents of the plasma miR-1 in AMI patients fell down nearly to the normal level at 14 days (P ＞ 0.05).There was no relevance between the expression of plasma miR-1 and the clinical characteristics of the study population (P ＞ 0.05).Moreover,ROC curve analyses demonstrated that miR-1 had the specificity and sensitivity for the diagnosis of early AMI,but was not superior to cTnT.Conclusions Our results showed that plasma miR-1 had the capacity in early diagnosis of early AMI,and can be biomarker for AMI,however,miR-1 is not superior to cTnT for the diagnosis of AMI.

Objective To study the effect of neuronal Nogo-66 receptor (NgR1) antagonist,soluble Nogo-66 receptor (sNgR1-Fc),on promoting the endogenous neural precursor cells (NPCs) differentiating into neurons in order to clarify the mechanism.Methods The cortical infarction was induced by photochemistry,named photothrombotic cortical injury (PCI).Twelve Sprague Dawley rats were randomly divided (random number) into three groups:Sham-operated group,PBS group,and sNgR1-Fc group.PBS (PBS group) or sNgR1-Fc (sNgR1-Fc group) was injected into the lateral ventricle of brain with a minipump.BrdU (Bromodeoxyuridine) was injected into the peritoneal cavity 4-6 days after PCI.The subdentate gyrus zone (SGZ) of brain from sacrificed rat was harvested for Immunohistochemistry to observe the ratio of NeuN +/BrdU + cells 35 days after PCI.Proteins including Nestin、Notch1 and Mash1 were detected by Western Blot.Results The cortical infarction in rat was successfully induced by photochemistry.Thirty-five days after PCI,the BrdU + cells number and theratio of NeuN +/BrdU + in the SGZ of the ipsilateral cerebrum hemisphere with PCI were significantly higher in sNgR1-Fc group than those in PBS group (P ＜ 0.05).The levels of Notch1,Mash1 and Neuro D in the sNgR1-Fc group were significantly higher than those in the PBS group (P ＜ 0.05),which were significantly higher than those in the Sham-operated group.Conclusions sNgR1-Fc could promote the endogenous NPCs differentiating into neurons in a cortical infarction model.The mechanisms may be attributed to the Notch/bHLH (proneural basic helix-loop-helix genes) signaling way.