Quantitative determination of paeoniflorin in paeonialbiflosides by HPLC was described. The average recovery was found to be 101.08%, and relativc standard deviations (RSD)1.90%. The calibration curve was linear in the range from 2.0?g/ml to 10.0?g/ml with r=0.9999. It was shown that the method is convenient, sensitive and with good reproducibility.

Objective To detect the levels of vascular endothelial growth factor (VEGF) in aqueous humor and vitreous of patients with neovascular glaucoma (NVG) and infer their possible effect on the development of neovascularization of iris. Methods The concentration of VEGF in 22 samples of ocular fluid of aqueous humor and vitreous respectively obtained from 11 patients with NVG undergone intraocular surgery were measured by using enzyme linked immunosobent assay (ELISA) for quantitative analysis. As control, 12 samples of ocular fluid of 6 patients with macular hole were detected by the same methods. Results The mean ?s VEGF concentrations in aqueous humor and vitreous from patients with NVG were [(1.451?0.247)?(1.610?0.125) ng/ml] higher than those in the cotrol group [(0.189?0.038)?(0.201?0.055) ng/ml], there was a significant difference between the two groups statistically ( t=12 007, P

Objective To evaluate the effect on the reversal of left ventricular aneurysm (LVA) and on heart function of percutaneous coronary intervention (PCI) therapy at different time of acute myocardial infarction (AMI). Methods A total of 326 patients with primary anterior AMI-accompanied LVA diagnosed by left ventriculography (LVG) from January 2001 to July 2004 were enrolled in this study. They were randomized into 4 groups according to the time of accepting PCI:≤3 h group, 4-6 h group, 7-12 h group and one week group. At the baseline and 6 months after AMI, the parameters of left ventricular diastolic volume index (LVEDVI), left ventricular systolic volume index (LVESVI), left ventricular ejection fraction (LVEF), left ventricular wall motion score (LVWMS) and left ventricular end diastolic pressure (LVEDP) were measured by LVG. The paradox volume index (PVI) was measured by equilibrium radionuclide at one week and 6 months after AMI.At 3 year following up to, the major adverse cardiac events (MACE) were recorded. Results At 6 months after PCI, the LVESVI, LVEDVI, WMS and LVEDP were all decreased while LVEF was increased in the four groups as compared with pre-PCl (P<0.05, respectively). Those parameters changed most obviously in ≤3 h group. At the 6th month after PCI, the PVI was lower in ≤3 h group (12.1±2.1)% than in 4-6 h, 7-12 h and one week group [(15.4±2.4)%, (16.5±2.5)% and (20.4±3.7)%, all P<0.05]. Within the 3 years follow-up, the MACE was significantly lower in 3 h, 4-6 h and 7-12 h groups than in one week group, and the mortality was lower too [(2.8%, 3.0% and 3.1% vs. 17.9%, all P<0.05]. Conclusions The early, fully and permanent open of the infraction-related artery can effectively inhibit the left ventricular remodeling process, prevent LVA formation, improve LV function and prognosis.

Objective To evaluate the role of activator protein-1 (AP-1) in the up-regulation of heme oxygenase-1 (HO-1) expression during lipopolysaccharide (LPS)-induced acute lung injury (ALI) in rats.Methods Forty-eight healthy male Sprague-Dawley rats,weighing 200-220 g,aged 2.5-3.0 months,were randomly divided into 4 groups (n=12 each): normal control group (group C),ALI group,curcumin + ALI group (group Cur+ ALI),and curcumin group (group Cur).In groups C and ALI,normal saline 0.5 ml and LPS 10 mg/kg (0.5 ml) were injected intravenously,respectively,30 min after 0.1％ dimethyl sulfoxide (the vehicle for curcumin) 0.5 ml was injected intraperitoneally.In groups Cur+ ALl and Cur,curcumin 20 mg/kg (0.5 ml) was injected intraperitoneally,and 30 min later LPS 10 mg/kg and normal saline 0.5 ml were injected,respectively.The rats were then sacrificed at 6 h after injection of LPS.The lungs were removed for microscopic examination.The pathological changes of the lung were scored.The malondialdehyde (MDA) content,superoxide dismutase (SOD)activity and expression of HO-1,AP-1 and HO-1 mRNA in lung tissues were determined.Results Compared with group C,the pathological score and MDA content were significantly increased,the SOD activity was significantly decreased,and the expression of HO-1,AP-1 and HO-1 mRNA was up-regulated in groups ALl and Cur +AL(l) (P ＜ 0.05),and no significant change was found in the parameters mentioned above in group Cur (P ＞ 0.05).The pathological score and MDA content were significantly higher,and the SOD activity and expression of HO-1,AP-1 and HO-1 mRNA were significantly lower in group Cur + ALl than in group ALI(P ＜ 0.05).Conclusion Transcription factor AP-1 activation is involved in the up-regulation of HO-1 expression during LPS-induced ALI in rats.

ObjectiveTo evaluate the role of p38MAPK signaling pathway in the up-regulation of heme oxygenase-1 (HO-1) expression in the lung tissue in rats with acute lung injury (AL1) induced by endotoxic shock.MethodsForty-eight male SD rats,aged 8 weeks,weighing 180-200 g,were randomly divided into 4 groups ( n =12 each):control group ( group C ) ; endotoxic shock group ( group LS );endotoxic shock +SB203580 (a specific p38MAPK inhibitor) group (group LSS) and SB203580 group (group SB).Normal saline 0.5ml was injected via the femoral vein in groups C and SB,while LPS 10 mg/kg (in 0.5 ml normal saline) was injected via the femoral vein in groups LS and LSS.When MAP was decreased to 75％ of baseline value,10％ dimethyl sulfoxide (DMSO) 0.1 ml was infused via the femoral vein in groups C and LS,while SB203580 5 mol/kg (in 10％ DMSO 0.1 ml) was infused via the femoral vein at a rate of 0.01 ml/min in groups LSS and SB.Arterial blood samples were obtained at 6 h after LPS or normal saline was given for blood gas analysis and oxygenation index (PaO2/FiO2) was calculated.Then the rats were sacrificed and the lungs were removed for microscopic examination.The pathological changes of the lung were scored.The lung water content was calculated.The MDA content,SOD activity,and expression of HO-1 mRNA and protein,p38MAPK protein and phospharylated p38MAPK (p-p38MAPK) protein were determined.ResultsCompared with group C,the oxygenation index and SOD activity were significantly decreased,the pathological score,lung water content and MDA content were significantly increased,and the expression of HO-1 mRNA and protein and p-p38MAPK protein was significantly up-regulated ( P＜0.05),while no significant change was found in p38MAPK protein expression in groups LS and LSS,and no significant change was found in the indexes mentioned above in group SB (P＞0.05).Compared with group LS,the oxygenation index and SOD activity were significantly increased,the pathological score,lung water content and MDA content were significantly decreased,the expression of HO-1 mRNA and protein was significantly up-regulated,and p-p38MAPK protein expression was down-regulated ( P＜0.05),and no significant change was found in p38MAPK protein expression in group LSS ( P＞0.05).ConclusionThe inhibition of p38MAPK signaling pathway can lead to the up-regulation of HO-1 expression in lung tissues in rats with ALI induced by endotoxic shock.

Objective To evaluate the effect of electro-acupuncture (EA) at Zusanli and Feishu on endotoxin shock-induced acute lung injury in rabbits.Methods Sixty healthy male New Zealand white rabbits aged 2 months weighing 1.5-2.0 kg were randomly divided into 6 groups (n =10 each):group sham operation (group S); group zinc protoporphyrin-Ⅸ (ZnPP-Ⅸ) (group Z); group lipopolysaccharide (LPS) (group L); group LPS + EA (group EL) ; group LPS + sham EA (group SEL) and group LPS + EA + ZnPP-Ⅸ (group ELZ).The animals were anesthetized with intraperitoneal 10％ chloral hydrate 400 mg/kg and tracheostomized.The animals kept spontaneous breathing.Right internal carotid artery was cannulated for BP monitoring.Ear vein was cannulated for drug administration.LPS 5 mg/kg was injected iv in groups L,EL,SEL,ELZ.Endotoxin shock was confirmed by decrease in BP by 20 ％ of the baseline value and PaO2/FiO2 ≤ 300.ZnPP-Ⅸ (heme oxygenase (HO-1 ) inhibitor)10μmol/kg was injected intraperitoneal at 2 h after LPS injection in groups Z and ELZ.Bilateral 15 min EA stimulation of Zusanli and Feishu ( according to atlas of animal acu-points) was performed once a day for 5 days before LPS administration in groups EL and ELZ.The animals were sacrificed by blood-letting at 6 h after LPS administration.The lungs were removed for microscopic examination (0 =no injury,4 =most severe injury),detection of alveolar epithelial cell apoptosis (by TUNEL) and determination of HO-1 protein and mRNA expression.Results LPS significantly increased lung injury scores,alveolar epithelial cell apoptosis index (the number of apoptotic cells/total cells) and HO-1 protein and mRNA expression.EA significantly attenuated lung injury and alveolar epithelial cell apoptosis induced by LPS and further increased the expression of HO-1 protein and mRNA in group EL as compared with group L.The protective effects of EA was counteracted by ZnPP- Ⅸ in group ELZ.Conclusion EA at Zusanli and Feishu can attenuate endotoxin shock-induced lung injury by up-regulation of HO-1 expression and inhibiting alveolar epithelial cell apoptosis in the lung.

Objective: To explore the effect of intravenous recombinant human brain natriuretic peptide (rhBNP) on regional myocardium deformability in patients with anterior acute myocardial infarction (AMI) after primary percutaneous coronary intervention (PCI). Methods: A total of 35 patients with anterior AMI who received primary PCI within 12 hours of symptom onset in our hospital from 2013-06 to 2013-12 were enrolled in this study and randomized into 2 groups: rhBNP group, the patients received intravenous rhBNP,n=18, Control group, the patients received standard intravenous nitrates,n=17, and the intravenous pumping administration maintained for 72 hours in both groups. The echocardiography was conducted at immediately, 7 days and 1 month after PCI respectively to compare the relative parameters. The occurrence of major adverse cardiac events (MACE) were followed-up for 6 months in all patients. Results: The baseline condition was similar between the two groups,P>0.05 , the parameters of echocardiography as LVEF and WMSI at immediately and 7 days after PCI were similar between the two groups,P>0.05. Compared with Control group, rhBNP group had the increased LVEF and decreased WMSI at 1 month after PCI ,P<0.05; rhBNP group had increased SRs at 7 days after PCI,P<0.05, while SRe and SRa were similar between the two groups,P>0.05; SRs, SEe and Sra were increased at 1 month after PCI, allP<0.05. The cTnI value in rhBNP group was lower than that in Control group as (50.09 ± 16.88) ng/ml vs (63.24 ± 18.60) ng/ml,P=0.036. The occurrence of MACE was similar between the two group,P>0.05. Conclusion: Intravenous administration of rhBNP could improve the regional myocardium deformability and the systolic/diastolic function in patients with anterior AMI after primary PCI.

Objective To evaluate the relationship between erythroid 2-related factor (Nrf2 )-antioxidant response element (ARE) pathway and acute lung injury (ALI) induced by endotoxic shock in rabbits .Methods Thirty healthy male New Zealand white rabbits ,aged 2 months ,weighing 1.5-2.0 kg ,were randomly divided into 3 groups (n=10 each) using a random number table :control group (group C) ,group ALI and all-trans retinoic acid group (group ATRA ) .In group ATRA ,all-trans retinoic acid 6 mg/kg (in filter sterilized vegetable oil 1.2 ml) was injected intraperitoneally once a day for 2 days .ALI was induced by lipopolysaccharide 5 mg/kg (in normal saline 2 ml ) injected via the auricular vein at 10 h after the last injection of ATRA in ALI and ATRA groups .The equal volume of normal saline was injected instead in group C .The rabbits were sacrificed at 6 h after lipopolysaccharide or normal saline administration .The pulmonary specimens were removed for determination of wet/dry lung weight ratio (W/D ratio ) and expression of Nrf2 mRNA and nuclear protein ,and HO-1 mRNA and protein in lung tissues .The pathological changes of lungs were scored .Results Compared with group C ,the pathological score and W/D ratio were significantly increased , and the expression of Nrf2 mRNA and nuclear protein ,and HO-1 mRNA and protein was up-regulated in ALI and ATRA groups ( P<0.05 ) .Compared with group ALI ,the pathological score and W/D ratio were significantly increased ,the expression of HO-1 mRNA and protein was down-regulated ( P<0.05) ,and no significant change was found in the expression of Nrf2 mRNA and nuclear protein in group ATRA ( P> 0.05 ) .Conclusion Activation of Nrf2-ARE pathway is the regulatory mechanism of the body adapting to the ALI induced by endotoxic shock in rabbits .

Objective To evaluate the method of establishment of a minipig model of ischemic heart failure(HF) with acute myocardial infarction(AMI) by coronary balloon occlusion and coadministration of injecting of microthrombi and plastic microspheres.Methods A total of eighteen minipigs were selected.After coronary angiography,angioplasty balloons were placed in the mid-distal of left anterior descending(LAD).The balloon was inflated intermittently to occlude the LAD 3 times and then to occlude it continuously for 120 minutes.After the balloon was taken out,4F Judkins-type angiogrphic catheter was superelectively engaged in LAD and 3 mL intermixture of mierothrombi and plastic microspheres were injected at 10 minites interval until TIMI myocardial perfusion was grade<2 and left ventfieular end-diastolic pressure was maintained from 15 to 18 mmHg.Electrocardiogram(ECG),hemodynamic perameters,ultrasonic cardiogram,cTnI and CK-MB were measured.Myocardial infarction area was evaluated by histopathology.Results Fourteen days later,fifteen minipigs survived and fourteen satisfied the criteria(pulmonary capillary wedge pressure.PCWP>18 mmHg and eardio output (CO) decreased beyond 30% ). The changes of ECG, hemodynamic perameters, CKMB, cTnI and cardiac pathologic examination were in accordance with AMI. Conclusion A stable experimental method of establishment of minipig model of ischemic heart failure (HF) with acute myocardial infarction (AMI) by coronary balloon occlusion and coadministration of injecting of microthrombi and plastic mierospheres is succeded. This method has advantages such as closed chest, higher success rate and stability compared with the drug induced, taehycardia-pacing induced, coronary artery ligation induced or microsphere injection alone methods.

Bronchial asthma is a type of complex causes of disease. It is determined by the environmen-tal factors and genetic factors,is caused by a variety of inflammatory cells in chronic inflammation of the air-way. More research has proved that T cells are involved in the main immune regulating airway inflammation. In recent years,studies have proved that the T cell activation induced apoptosis mechanisms involved in the patho-genesis ofasthma,based on T cell apoptosis in bronchial asthma onset process is summarized,and provide the ba-sis for further elucidate the pathogenesis of asthma.