Objective To investigate differential expressed protein in the intestinal mucosa of patients with inflammatory bowel disease (IBD) with antibody chips,and to explore the possible role of the screened proteins in pathogenesis of IBD.Methods The mucosa tissues of nine patients with ulcerative colitis (UC),nine patients with Crohn's disease (CD) and nine control individuals were collected.After total protein of each group was extracted,the differential expressed protein of each group was analyzed by Raybiotech L-series human cytokine antibody chips.The mucose tissues of other nine patients with UC,nine patients with CD and nine control individuals were collected,and were used to verify the greatly differential expressed proteins by Western blot.The t-test was performed to compare two groups.Results Compared with the control group,there was significantly difference in 263 cytokines of UC group,and 414 cytokines of CD group.And then the higher expressions of herpes virus entry mediator,leukemia inhibitory factor and platelet factor 4 in the mucosa tissues of IBD patients were confirmed by Western blot and the differences were statistically significant (UC:t=23.85,9.53,18.88; CD:t=13.54,16.65,13.67,all P＜0.01).Conclusion The screened differential expressed cytokines in the mucosa tissues of IBD patients by cytokine antibody chips could be helpful to reveal the pathogenesis of IBD and discover new molecular biomarkers.

Objective To compare the roles of Toll-like receptor 4 (TLR4)/NF-κB signal pathway in acute lung injury (ALl) induced by blunt chest trauma and by blunt chest trauma-hemorrhagic shock and resuscitation (double hits) in rats.Methods Forty male Sprague-Dawley rats,aged 8 weeks,weighing 240-280 g,were randomly assigned into 3 equal groups (n =10 each) using a random number table:sham operation group (S group),blunt chest trauma group (T group),and blunt chest trauma and hemorrhagic shock and resuscitation group (group THSR).Lung contusion was induced in anesthetized rats by dropping a 300 g weight onto a precordial protective shield to direct the impact force away from the heart and toward the lungs.Blood was withdrawn via the femoral artery 5 min later until MAP was decreased to 35-45 mmHg within 15 min and maintained at this level for 60 min,followed by resuscitation.At 6 h after the model was established,the arterial blood samples were collected for blood gas analysis and detection of tumor necrosis factor-alpha (TNF-α) concentrations in serum.Oxygenation index (PaO2/FiO2) was calculated.The rats were then sacrificed and pulmonary specimens were obtained for determination of TLR4 expression and NF-κB ac tivity (by immunohistochemistry and Western blot) in lung tissues and for microscopic examination.Results Compared with group S,PaO2 and PaO2/FiO2 were significantly decreased,PaCO2 and TNF-α concentrations in serum were increased,TLR4 expression was up-regulated,and NF-κB activity was enhanced in T and THSR groups (P ＜ 0.05).Compared with group T,PaO2 and PaO2/FiO2 were significantly decreased,PaCO2 and TNF-α concentrations in serum were increased,TLR4 expression was up-regulated,and NF-κcB activity was enhanced in THSR group (P ＜ 0.05).The histopathological damage to lung tissues was aggravated in THSR group as compared with T group.Conclusion The role of TLR-4/NF-κB signal pathway in ALI induced by blunt chest traumahemorrhagic shock and resuscitation (double hits) is significantly stronger than that in ALI induced by blunt chest trauma alone in rats.

This study reported the analysis of plasma phospholipid metabolism of the rats and the pathological biomarkers between the type 2 diabetes model control group (MC) and the normal control group (NC). SD rats were randomly divided into 2 groups: NC and MC. To investigate state of plasma metabolite profiling in normal body, type 2 diabetes mellitus (T2DM) model group using UPLC-Q-TOF/MS which was used as analysis tool in this research. The compounds were identified by UPLC-Q-TOF/MS based on MS/MS fragment ions information, element composition in MassLynx 4.1 and the Lipid Maps database. The sign of two groups of samples in specific markers for screening was through a software package in R software (BioMark software). The results show that the pathological markers were mainly phosphatidylcholine (PC) and triglycerides (TG); the 2-acyl PC in the MC group was less more obviously than that in the NC group; high carbon number and high degree of unsaturation of the TG was reduced under the condition of type 2 diabetes. In the state of type 2 diabetes, metabolic changes occurred in rat plasma phospholipids obviously, which had a close relationship with the occurrence and development of T2DM.

Objective To explore the relationship between quality of life and knowledge,beliefs,behavioral,pulmonary function outcomes in stable-stage patients with chronic obsturctive pulmonary disease (COPD).Methods Using the general data questionnaire,COPD assessment test (CAT),knowledge,attitude and behavior questionnaire to investigate 93 stable-stage COPD patients in urban and rural areas,and measure the level of forced expiratory volume in one second (FEV1％).Results CAT total score was (22.56 ± 6.40) points which was in severe level;knowledge,beliefs,behavior total score was (41.94 ± 8.20) points,and FEV1％ was (59.81 ± 7.64) ％.The CAT was negatively correlated with knowledge,beliefs,behavior total score and two dimensions of beliefs,behavior and FEV1％,r values were-0.262,-0.288,-0.217,-0.256 respectively,P ＜ 0.05.Conclusions The COPD patients in stable-stage have a high level of CAT.Targeted invention should be combined with the status of the knowledge,beliefs and behavior to improve the level of air flow,and quality of life of patients.

Background:Studies showed that neuropeptide S receptor 1(NPSR1)gene polymorphisms were associated with the susceptibility of inflammatory bowel disease( IBD)in Europe’s populations,however,there is no study on the relevance in Chinese population. Aims:To investigate the association of NPSR1 gene polymorphisms with IBD in Chinese Han population. Methods:A total of 457 IBD patients[355 cases of ulcerative colitis(UC)and 102 cases of Crohn’s disease ( CD)]from Zhongnan Hospital of Wuhan University and 500 healthy controls were recruited. Genotyping of 2 single nucleotide polymorphisms(SNPs)of NPSR1,rs323922(C→G mutation)and rs740347(G→C mutation)was performed by using PCR and sequencing techniques. Results:Differences of the frequencies of genotypes and alleles for rs323922 and rs740347 between UC,CD patients and controls didn’t reach statistical significance(P >0. 05). Genotype-phenotype analysis showed that there were some impact of genotypes for rs323922 and rs740347 on clinical phenotypes of IBD:( i) For rs323922,mutant CG genotype was correlated with male CD patients(OR:0. 441,95% CI:0. 230-0. 844)and CD involving the colon(OR:0. 425,95% CI:0. 199-0. 911),and might be a protective factor.(ii)For rs740347,mutant CC genotype was correlated with early onset CD patients( <16 years old)(OR:15. 019,95% CI:2. 634-86. 470)and mutant C allele was correlated with CD involving the colon(OR:2. 142,95% CI:1. 709-4. 294),both were risk factors. Conclusions:Polymorphisms of NPSR1 rs323922 and rs740347 are not contributors of IBD susceptibility in Chinese Han population,but might be correlated with some clinical phenotypes of IBD.

Objective To compare the roles of inflammatory response in acute lung injury (ALI) induced by blunt chest trauma verus by blunt chest trauma-hemorrhagic shock and resuscitation (double hits) in rats.Methods Thirty male Sprague-Dawley rats,aged 8 weeks,weighing 240-280 g,were randomly assigned into 3 equal groups (n =10 each) using a random number table:sham operation group (S group),blunt chest trauma group (T group),and blunt chest trauma and hemorrhagic shock and resuscitation group (THSR group).Lung contusion was induced in anesthetized rats by dropping a 300 g weight onto a precordial protective shield to direct the impact force away from the heart and toward the lungs.Blood was withdrawn via the left femoral artery 5 min later until MAP was decreased to 35-45 mmHg within 15 min and maintained at this level for 60 min,followed by resuscitation.At 6 h after the model was established,the arterial blood samples were collected for blood gas analysis and detection of serum concentrations of tumor necrosis factor-α (TNF-α),interleukin-6 (IL-6),IL-1β and IL-10 (by ELISA).The rats were then sacrificed and pulmonary specimens were obtained for determination of contents of TNF-α,IL-6,IL-1β and IL-10 in lung tissues and for microscopic examination.Results Compared with group S,PaO2 was significantly decreased,and the levels of TNF-α,IL-6,IL-1β and IL-10 in serum and lung tissues were increased in T and THSR groups.Compared with group T,PaO2 was significantly decreased,and the levels of TNF-α,IL-6,IL-1β and IL-10 in serum and lung tissues were increased in group THSR.The histopathological damage to lung tissues was aggravated in THSR group as compared with T group.Conclusion The role of inflammatory response in ALI induced by blunt chest trauma-hemorrhagic shock and resuscitation (double hits) is significantly stronger than that in ALI induced by blunt chest trauma alone in rats.

Objective To evaluate the relationship between DJ?1 and diabetes mellitus ( DM )?caused influence on cardioprotection induced by ischemic postconditioning in rats. Methods Adult male Sprague?Dawley rats, aged 3 months, weighing 220-250 g, were used in the study. DM was induced by intraperitoneal injection of 1% streptozotocin 60 mg∕kg and confirmed by blood glucose≥16.7 mmol∕L. Forty?eight rats with DM were randomly divided into 3 groups ( n=16 each) using a random number table:sham operation group ( group DM?S ) , myocardial ischemia?reperfusion ( I∕R ) group ( DM?IR ) and ischemic postconditioning group (DM?IPO group). Another 48 normal rats received the equal volume of citrate buffer solution instead and served as control. Those rats were randomly divided into 3 groups ( n=16 each) using a random number table: sham operation group ( S group) , myocardial I∕R group ( IR group) and ischemic postconditioning group (IPO group). At 12 weeks after streptozotocin injection, myocardial I∕R was produced by 30 min occlusion of the left anterior descending branch of the coronary artery followed by 120 min reperfusion. Ischemic postconditioning was induced by 3 cycles of 10 s reperfusion followed by 10 s limb ischemia at the end of 30 min limb ischemia. At 120 min of reperfusion, the animals were sacrificed, and hearts were removed for determination of myocardial infarction size ( using TTC ) , and expression of DJ?1, phosphatase and tensin homologue ( PTEN) protein, and phosphorylated Akt ( p?Akt) in myocardial tissues ( by Western blot) . Results The infarction size was significantly increased in diabetic and nondiabetic rats during myocardial I∕R. The expression of DJ?1, PTEN protein and p?Akt was significantly higher during myocardial I∕R in nondiabetic rats, and the expression of PTEN protein and p?Akt was up?regulated, and no significant change was found in DJ?1 expression during myocardial I∕R in diabetic rats. Ischemic postconditioning reduced infarction size during myocardial I∕R and up?regulated the expression of DJ?1 and p?Akt, and down?regulated the expression of PTEN protein in nondiabetic rats, but not in diabetic rats. Compared with nondiabetic rats, the expression of DJ?1 and p?Akt was down?regulated, and the expression of PTEN protein was up?regulated after ischemic postconditioning in diabetic rats. Conclusion The mechanism by which DM abolishes cardioprotection induced by ischemic postconditioning is associated with down?regulation of DJ?1 expression in rats.

Objective To investigate the effects of penehyclidine hydrochloride on activities of nuclear factor kappa B (NF-kB) and activator protein-1 (AP-1) during actue lung injury induced by blunt chest trauma-hemorrhagic shock and resuscitation (HSR) in rats.Methods Thirty male Sprague-Dawley rats,aged 8 weeks,weighing 250-300 g,were randomly assigned into 3 equal groups (n =10 each) using a random number table:sham operation group (group S),blunt chest trauma-HSR group (group THSR) and penehyclidine hydrochloride group (group PHCD).The model of actue lung injury induced by blunt chest trauma-HSR was induced by dropping a 300 g weight onto a precordium in anesthetized rats.Blood was withdrawn via the femoral artery 5 min later until MAP was decreased to 35-45 mmHg within 15 min and maintained at this level for 60 min,followed by resuscitation.In PHCD group,PHCD 2 mg/kg was injected intravenously at 60 min after hemorrhagic shock.At 6 h after the model was established,blood samples were obtained for measurement of concentrations of tumor necrosis factor-alpha (TNF-α) in serum.The lungs were then removed for determination of lung water content,myeloperoxidase (MPO) activaty (by colorimetric assay),NF-κB and AP-1 activaties (using electrophoretic mobility shift assay) in lung tissues,and for microscopic examination of pathologic changes (under light microscope).The left lung was lavaged,and lung permeability index (LPI) was calculated.Results Compared with S group,lung water content,LPI,serum TNF-α level and activites of MPO,NF-κB and AP-1 were significantly increased in THSR and PHCD groups.Compared with THSR group,lung water content,LPI,serum TNF-α concentrations and activites of MPO,NF-κB and AP-1 were significantly decreased in PHCD group.The pathological damage to lung tissues was significantly reduced in PHCD group as compared with THSR group.Conclusion PHCD can inhibit activities of NF-κB and AP-1 in lung tissues,thus mitigating acute lung injury induced by blunt chest trauma-HSR in rats.

This study reported the analysis of plasma phospholipid metabolism of the rats and the pathological biomarkers between the type 2 diabetes model control group (MC) and the normal control group (NC). SD rats were randomly divided into 2 groups: NC and MC. To investigate state of plasma metabolite profiling in normal body, type 2 diabetes mellitus (T2DM) model group using UPLC-Q-TOF/MS which was used as analysis tool in this research. The compounds were identified by UPLC-Q-TOF/MS based on MS/MS fragment ions information, element composition in MassLynx 4.1 and the Lipid Maps database. The sign of two groups of samples in specific markers for screening was through a software package in R software (BioMark software). The results show that the pathological markers were mainly phosphatidylcholine (PC) and triglycerides (TG); the 2-acyl PC in the MC group was less more obviously than that in the NC group; high carbon number and high degree of unsaturation of the TG was reduced under the condition of type 2 diabetes. In the state of type 2 diabetes, metabolic changes occurred in rat plasma phospholipids obviously, which had a close relationship with the occurrence and development of T2DM.
Animals ; Biomarkers ; blood ; Chromatography, High Pressure Liquid ; Diabetes Mellitus, Experimental ; blood ; Diabetes Mellitus, Type 2 ; blood ; Metabolome ; Phospholipids ; blood ; Rats ; Rats, Sprague-Dawley ; Tandem Mass Spectrometry