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onto a precordial protective shield to direct the impact force away from the heart and toward the lungs.Blood was withdrawn via the femoral artery 5 min later until MAP was decreased to 35-45 mmHg within 15 min and maintained at this level for 60 min,followed by resuscitation.At 6 h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.

Objective To evaluate the role of pretreatment with docosahexaenoic acid (DHA) in the protective effect of angiopoietin-1 (Ang-1) on rat brain microvascular endothelial cells (BMVECs) during oxygen glucose deprivation (OGD).Methods BMVECs were sub-cultured in vitro and divided with a random number table into 7 groups:normal control group,normal control + Ang-1 group,OGD group,OGD + Ang-1 group,OGD + DHA group,OGD + DHA + Ang-1 group,and OGD + DHA + GW9662 + Ang-1 group.The normal control and normal control + Ang-1 groups were cultured in DMEM containing serum,5 mmol/L glucose,and 1.25 mmol/L pyruvate;OGD groups were cultured in glucose-and serum-free DMEM.DHA (40 μmol/L) was added to OGD + DHA,OGD + DHA + Ang-1,and OGD + DHA + GW9662 + Ang-1 groups,and 5 μmol/LGW9662 [inhibitor of peroxisome proliferator-activated receptor gamma (PPAR-γ)] to OGD + DHA + GW9662 +Ang-1 group,before pretreatment for 1 hour in 5％ CO2 and 95％ air.After the pretreatment,Ang-1 (250 ng/ml)was added to normal control + Ang-1,OGD + Ang-1,OGD + DHA + Ang-1,and OGD + DHA + GW9662 +Ang-1 groups.The cells were cultured in 94％ N2∶ 5％ CO2∶ 1％ O2 for 24 hours,except for normal control and normal control + Ang-1 groups,which were cultured in 5％ CO2 and 95％ air instead.The cell apoptosis rate was detected with flow cytometry,expressions of Bax,Bcl-2,caspase-3,Tie-1,Tie-2,pTie-2,pAkt,ZO-1proteins with Western blot.Results Compared with normal control group,the cell apoptosis rate in OGD,OGD + Ang-1,OGD + DHA,OGD + DHA + Ang-1,and OGD + DHA + GW9662 + Ang-1 groups were significantly increased (P =0.000,0.000,0.000,0.004,0.000);the expression levels of Bax,caspase-3,and Tie-1 were significantly enhanced (Bax:0.62 ± 0.03,0.38 ± 0.03,0.45 ± 0.03,0.26 ± 0.02,0.33 ± 0.02vs.0.16 ±0.01;caspase-3:0.76 ±0.05,0.42 ±0.04,0.52 ±0.02,0.32 ±0.02,0.40 ±0.02 vs.0.15 ±0.01;Tie-1:0.51 ±0.03,0.25 ±0.01,0.33 ±0.02,0.16±0.01,0.22±0.02 vs.0.12 ±0.01;all P=0.000);the expression levels of Bcl-2,Bcl-2/Bax,Tie-2,and pTie-2 were significantly decreased [Bcl-2:0.09±0.01,0.20±0.01,0.16±0.02,0.31±0.01,0.22±0.01 vs.0.34±0.01;Bcl-2/Bax:(14.93±1.86)％,(68.03±5.56)％,(36.93 ±2.22)％,(119.1 ±13.3)％,(64.23 ±6.07)％ vs.(208.33 ±7.37)％;Tie-2:0.07±0.01,0.16±0.02,0.11 ±0.01,0.21±0.01,0.18±0.01 vs.0.26±0.01;pTie-2:0.05±0.01,0.15 ±0.01,0.07 ±0.01,0.22 ±0.02,0.16±0.01 vs.0.27 ±0.01;allP=0.000],in addition,pAkt and ZO-1 in OGD,OGD + Ang-1,OGD + DHA,and OGD + DHA + GW9662 +Ang-1 groups were also significantly reduced (pAkt:0.13 ±0.01,0.26 ±0.01,0.14 ±0.01,0.28 ±0.02vs.0.39±0.02;ZO-1:0.08±0.01,0.18±0.01,0.10±0.01,0.19±0.01vs.0.23±0.02;allP=0.000).Compared with the OGD group,OGD + Ang-1 and OGD + DHA + Ang-1 groups demonstrated significantly reduced cell apoptosis (both P =0.000).Compared with normal control + Ang-1 group,the expression levels of pTie-2,pAkt,and ZO-1 were significantly decreased in OGD + Ang-1 and OGD + DHA +Ang-1 groups (pTie-2:0.15 ±0.01,0.22 ±0.02 vs.0.52 ±0.02;pAkt:0.26 ±0.01,0.37 ±0.04 vs.0.67 ± 0.05;ZO-1:0.18 ± 0.01,0.24 ± 0.02 vs.0.39 ± 0.05;all P =0.000).Compared with OGD +Ang-1 group,OGD + DHA + Ang-1 group had significantly decreased cell apoptosis and expression levels of Bax,caspase-3 and Tie-1,and significantly increased expressions of Bcl-2,Bcl-2/Bax,Tie-2,pTie-2,pAkt,and ZO-1 (all P =0.000),while OGD + DHA + GW9662 + Ang-1 group showed no significant differences in these indexes (P =0.202,0.770,0.382,0.448,0.233,0.736,0.143,0.526,0.495,0.670).Conclusion Pretreatment with DHA may enhance the protective effect of Ang-1 on rat BMVECs under the condition of OGD,possibly via activating PPAR-γ,suppressing Tie-1 expression,and hence amplifying the activation of Tie-2.

To explore the relationships between traditional Chinese medicine (TCM) constitutional types and overweight or obesity so as to provide evidence for adjusting constitutional bias and preventing and treating obesity.

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.

Boronic acids and their derivatives have been widely used in carbohydrate-sensitive materials because they can selectively bind 1,2-and 1,3-diol compounds, including sugars, to form cyclic boronate esters. In this work, pheylboronic acid ( PBA) moieties were grafted onto the backbone of poly( acrylic acid) ( PAA) through the condensation reaction between aminopheyl-boronic acid and carboxylic acid group of PAA in the presence of EDC/NHS, designed as PAA-PBA. Then the resulting PAA-PBA were assembled with poly ( ethyleneimine) ( PEI) to form PAA-PBA multilayer films. The sensing performance of the PEI/PAA-PBA film to carbohydrate (> 50 μg/mL ) , including glucose, fructose, mannose and galactose, has been investigated by combination of the complementary techniques of quartz crystal microbalance ( QCM ) and atomic force microscopy ( AFM) . It was demonstrated that the multilayer showed higher sensitivity to fructose than glucose, mannose and galactose. The interferences of ascorbic acid, uric acid and dopamine to the recognition of glucose can be avoided and the multilayer sensor with excellent long term stability can be recycled by changing pH value of buffer solutions. This system may be potential in realization of high selectivity and high sensitivity sensing system for probing carbohydrate.

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.

Objective To evaluate the mechanism of reduction of protection induced by hypoxic postconditioning (HPO) in diabetic myocardiocytes subjected to hypoxia-reoxygenation (H/R),and the relationship with DJ-1 expression.Methods H9c2 cells cultured in normal culture atmosphere were randomly divided into 6 groups (n=36 each) using a random number table:control group (group C),group H/R,group HPO,plasmid carrying DJ-1 gene transfection group (group D),plasmid carrying DJ-1 gene transfection + H/R group (group DH),and plasmid carrying DJ-1 gene transfection + H/R + HPO group (group DHH).H/R was induced by 4 h of hypoxia followed by 2 h of reoxygenation.H9c2 cells were cultured in high glucose culture medium (30 mmol/L) for 48 h in C,H/R and HPO groups.H/R model was established in H/R and HPO groups.HPO was induced by 3 cycles of 5 min reoxygenation and 5 min hypoxia before the onset of reoxygenation in group HPO.In D,DH and DHH groups,the plasmid carrying DJ-1 gene (pEX-2-EGFP-DJ-1) was transfected into the cells,and then the cells were cultured in high glucose culture medium and subjected to H/R and HPO,respectively.At 2 h of reoxygenation,the cell survival rate was measured using the cell counting kit-8 assay,and the level of lactate dehydrogenase (LDH) in the supernatant was detected by enzyme-linked immunosorbent assay,the autophagosomes were examined with a transmission electron microscope,and the expression of DJ-1 and p62 and ratio of microtubule-associated protein 1 light chain 3 Ⅱ / Ⅰ (LC3 Ⅱ / Ⅰ) in cells were detected by Western blot.Results Compared with group C,the cell survival rate and DJ-1 expression were significantly decreased,and the LDH activity was significantly increased in H/R and HPO groups (P＜0.01).There was no significant difference in the parameters mentioned above between H/R and HPO groups (P＞0.05).Compared with group D,the cell survival rate was significantly decreased,and the LDH activity was significantly increased in group DH (P＜0.01).Compared with group DH,the cell survival rate,the number of autophagosomes and LC3 Ⅱ / Ⅰ ratio were significantly increased,and the LDH activity and p62 expression were significantly decreased in group DHH (P＜0.01).There was no significant difference in the parameters mentioned above between H/R and DH groups (P＞0.05).Conclusion The mechanism of reduction of protection induced by HPO in diabetic myocardiocytes subjected to H/R is related to high glucose-induced inhibition of DJ-1 expression and decrease in autophagy.

Objective To evaluate the role of phosphatase and tensin homologue deleted on chromosome 10 (PTEN) in diabetes mellitus-induced reduction of hypoxic postconditioning (HPO)-induced protection of cardiomyocytes and the relationship with glycogen synthase kinase-3β (GSK-3β)-mediated mitochondrial apoptotic pathway.Methods H9c2 cells incubated in high-glucose (30 mmol/L) medium for 24 h were divided into 6 groups (n =5 each) using a random number table:normoxia group (group N),hypoxia-reoxygenation (H/R) group,group HPO,PTEN gene silencing normoxia group (group P-N),PTEN gene silencing H/R group (group P-H/R),and PTEN gene silencing HPO group (group P-HPO).H9c2 cells were exposed to 95％ N2-5％ CO2 for 4 h followed by 2 h reoxygenation with 90％ O2-10％ CO2.HPO was induced by 3 cycles of 5 min reoxygenation followed by 5 min hypoxia before reoxygenation.At the end of reoxygenation,the level of lactate dehydrogenase (LDH) in the supernatant was detected by enzyme-linked immunosorbent assay,the changes in mitochondrial membrane potential (MMP were assessed by JC-1 fluorescence assay,the cell apoptosis was detected by AnnexinV-FITC/PI flow cytometry,and the expression of PTEN and phosphorylated GSK-3β (p-GSK-3β) was determined by Western blot.The JC-1 monomer/polymer ratio and apoptosis rate were calculated.Results Compared with group N,the amount of LDH released,JC-1 monomer/polymer ratio and apoptosis rate were significantly increased,and the expression of PTEN was up-regulated in H/R and HPO groups (P＜0.05).There was no significant difference in the parameters mentioned above between group H/R and group HPO (P＞0.05).Compared with group HPO,the amount of LDH released,JC-1 monomer/polymer ratio and apoptosis rate were significantly decreased,PTEN expression was down-regulated,and the expression of p-GSK-3β was up-regulated in group P-HPO (P＜0.05).Compared with group N,the expression of PTEN was significantly down-regulated,and no significant changes were found in the other parameters mentioned above in group P-N (P＞0.05).Compared with group H/R,the expression of PTEN was significantly down-regulated,and no significant changes were found in the other parameters mentioned above in group P-H/R (P＞0.05).Conclusion PTEN is involved in diabetes mellitus-induced reduction of HPO-induced protection of cardiomyocytes,and the mechanism is associated with PTEN-induced activation of GSK-3β-modulated mitochondrial apoptotic pathway.

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.

Cross-Sectional Studies ; Depression/epidemiology* ; Humans ; Job Satisfaction ; Occupational Stress/epidemiology* ; Oil and Gas Fields ; Stress, Psychological ; Surveys and Questionnaires