OBJECTIVE: To compare TLC fingerprints between different batches of compound Herba taraxaci enemas (CHTE) ant to lay a foundation for establishing a more stable preparation technics and quality standards for CHTE. METHODS: The chloroform extract of 2 batches of CHTE were chromatographed by TLC and the samples were scanned by TLC scanner at a single wavelength of 280nm,the difference between different batches was compared. RESULTS: The TLC of chloroform extracts was well-separated,there were 6 common peaks and 2 non-common peaks in the TLC of 2 batches of samples, with some of the peaks identified in terms of the medicinal material categories, but there was a significant difference in contents among the common peaks. CONCLUSIONS: It was hard to guarantee the relative conformity in numbers of components and the contents between different batches of preparations,the preparation technics and quality standard of raw materials remain to be further optimized and the quality standard for Chinese herb medicinal preparations in hospital should be improved further.

CT and TT genotype frequencies of TNF-? gene at -857 site in obese patients with type 2 diabetes mellitus (DM)andcontrolgroupswithoutobesity were 0.396, 0.020 and 0.179, 0.000, and T allele 0.220 and 0.090, respectively. This finding suggests that mutation is associated with type 2 DM in obese subjects.

Objective To evaluate the effects of Janus kinase 2/signal transducers and activators of transcription 3 (JAK2/STAT3) signaling pathway on the brain injury induced by myocardial ischemia-reperfusion (I/R) in diabetic rats.Methods Pathogen-free male Sprague-Dawley rats,weighing 200-220 g,were used in this study.Diabetes mellitus was induced by intraperitoneal 1％ streptozotocin 60 mg/kg and confirmed by blood glucose level ≥ 16.7 mmol/L 3 days later.Twenty-four rats with diabetes mellitus were randomly allocated into 3 groups (n =8 each) using a random number table:sham operation group (group S),I/R group,and myocardial I/R + AG490 (JAK inhibitor) group (group ⅠA).Myocardial I/R was induced by occlusion of the anterior descending branch of the left coronary artery for 30 min,followed by 120 min of reperfusion in the rats anesthetized with pentobarbital sodium.AG490 3 mg/kg was injected intravenously at 20 min before reperfusion in group IA.The rats were sacrificed at 120 min of reperfusion,and the brains were removed for determination of caspase-3 and nuclear factor kappa B (NF-κB) activities (using colorimetric method),cell apoptosis (by TUNEL),and expression of interleukin-1 (IL-1),IL-6,IL-8,Bax,Bcl-2,cytochrome C (Cyt c),phosphorylated JAK2 (p-JAK2),and phosphorylated STAT3 (p-STAT3) (by Western blot).Apoptosis index was calculated.Results Compared with group S,the expression of Bax,Cyt c,IL-1,IL-6,IL-8,p-JAK2 and p-STAT3 was significantly up-regulated,the expression of Bcl-2 was down-regulated,and NF-κB and caspase-3 activities and apoptosis index were increased in I/R and IA groups (P＜0.05).Compared with group I/R,the expression of Bax,Cyt c,IL-1,IL-6,IL-8,p-JAK2 and p-STAT3 was significantly down-regulated,the expression of Bcl-2 was up-regulated,and NF-κB and caspase-3 activities and apoptosis index were decreased in group IA (P＜0.05).Conclusion Inflammatory responses mediated by JAK2/STAT3 signaling pathway are involved in the brain injury induced by myocardial I/R in diabetic rats.

Objective To evaluate the effects of ulinastatin on perioperative inflammatory response during cardiopulmonary bypass. Methods Comprehensive search of PubMed,EMbase,the Cochrane Library,CECDB,CQVIP,CNKI databases was conducted for randomized controlled trials(RCTs) published from January 1994 to June 2014.The included studies were evaluated strictly and the extracted data were analyzed by RevMan 5.2. Results A total of 7 RCTs including 335 patients were included,and 154 patients were in the experimental group,while 181 patients were in the control group.In the experimental group, patients were given Ulinastatin during surgery. System evaluation results show that, the concentration of TNF-α [ SMD (95%CI) were -3.48(-4.64,-2.31)] and IL-6 [SMD(95%CI) were -3.04(-4.54,-1.54)] in experimental group at 1 h after weaning from CPB were significantly lower than those in control group. Conclusion Ulinastatin used perioperatively in cardiopulmonary bypass can significantly reduce postoperative inflammation.

Objective To investigate the correlation between the serum ferritin levels and the post-stroke depression (PSD). Methods From July 2014 to October 2015, the inpatients with the first-ever acute ischemic stroke were colected consecutively. Chemiluminescence microparticle immune assay was used to measure the serum ferritin levels within 24 h after admission. Depressive symptoms were screened by using the 17-item Hamilton depression scale (HAMD-17) at 3 months after onset. In patients with a HAMD-17 score ≥7, the depression was further diagnosed according to The Diagnostic and Statistical Manual of Mental Disorders, 4th edition. Results A total of 200 patients with the first-ever acute ischemic stroke were enroled, 55 (27. 5% ) of them were diagnosed as PSD. There were significant differences in the body mass index (BMI), years of education, waist circumference, high sensitive-C-reactive protein, homocysteine, National Institutes of Health Stroke Scale score (at baseline, discharge, and day 90), mRs score (at discharge and day 90), BI (at discharge and day 90), and the proportions of widowed or solitary patients between the PSD group and the non-PSD group (al P < 0. 05 ). The serum ferritin level in the PSD group was significantly higher than that in the non-PSD group ( median [ interquartile range], 261. 90[142. 10-364. 90] μg/L vs. 164. 40[132. 50- 195. 10] μg/L; Z = - 4. 814, P < 0. 001 ). Multivariate logistic regression analysis adjusted for confounding factors showed that the baseline serum ferritin level >136. 375 μg/L was an independent risk factor for PSD (odds ratio 1. 041 per 1-quartile increase, 95%confidence interval 1. 009-1. 239; P = 0. 045). Conclusions The elevated baseline serum ferritin level is associated with PSD.

Objective To investigate the effects of penehyclidine hydrochloride (PHC) on acute lung injury induced by blunt chest trauma-hemorrhagic shock and resuscitation in rats.Methods Forty male SpragueDawley rats,aged 8 weeks,weighing 250-300 g,were randomly assigned into 4 equal groups (n =10 each) using a random number table:sham operation group (S group),blunt chest trauma combined with hemorrhagic shock and resuscitation group (group THSR),PHC for prevention group (group P1)and PHC for treatment group (group P2).ALI was induced by dropping a 300 g weight onto a precordial protective shield to direct the impact force away from the heart and toward the lungs in anesthetized rats in THSR,P1 and P2 groups.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 P1 group,PHC 2 mg/kg was injected intravenously at 30 min before blunt chest trauma.In P2 group,PHC 2 mg/kg was injected intravenously at 60 min after hemorrhagic shock.At 6 h after the model was established,arterial blood samples were obtained for blood gas analysis and for measurement of concentrations of interleukin-6 (IL-6) and interleukin-1β (IL-1β) in serum by ELISA.Oxygenation index (OI) was calculated.The animals were sacrificed and bronchoalveolar lavage fluid (BALF) was collected for determination of white blood cell count and protein concentrations.Lungs were removed for examination of pathological changes and ultrastructure and for determination of Toll-like receptor (TLR4) and phosphor-p38 mitogen activated protein kinase (p-p38MAPK) expression (by Western blot).Results Compared with group S,PaO2 and OI were significantly decreased,PaCO2,protein concentrations in BALF,white blood cell count,and IL-6 and IL-1β concentrations in serum were increased,and TLR4 and p-p38MAPK expression was up-regulated in THSR,P1 and P2 groups.Compared with group THSR,PaO2 and OI were significantly increased,PaCO2,protein concentrations in BALF,white blood cell count,and IL-6 and IL-lβ concentrations in serum were decreased,TLR4 and p-p38MAPK expression was down-regulated in P1 and P2 groups.No significant differences were found in the parameters mentioned above between P1 and P2 groups.Conclusion PHC can mitigate acute lung injury induced by blunt chest trauma-hemorrhagic shock and resuscitation in rats,and inhibited activation of TLR4/ p38MAPK signaling pathway and attenuated inflammatory responses are involved in the mechanism.

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 investigate the effects of penehyclidine hydrochloride on Fas/FasL expression during acute lung injury induced by blunt chest trauma-hemorrhagic shock and resuscitation (HSR) in rats.Methods Thirty male SPF Sprague-Dawley rats, aged 8 weeks, weighing 245-275 g, were randomly assigned into 3 equal groups using a random number table: sham operation group (group Sham) , blunt chest trauma-HSR group (group THSR) and penehyclidine hydrochloric group (group PHCD).The model of acute 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 mean arterial pressure 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, the rats were sacrificed, the lungs were then removed for microscopic examination of pathologic changes and for determination of Fas, FasL and caspase-8 expression, and interleukin-6 (IL-6) and IL-1β contents in lung tissues.Apoptotic index was calculated.Results Compared with group Sham, the expression of Fas, FasL and caspase-8 was significantly up-regulated, and AI and contents of IL-6 and IL-1β were increased in THSR and PHCD groups (P＜O.05).Compared with group THSR, the expression of Fas, FasL and caspase-8 was significantly down-regulated,and AI and contents of IL-6 and IL-1β were decreased in group PHCD (P＜0.05).The pathologic changes of lungs were significantly reduced in group PHCD compared with group THSR.Conclusion The mechanism by which penehyclidine hydrochloride inhibits lung cell apoptosis induced by blunt chest trauma-HSR is associated with inhibition of Fas/FasL expression 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.