This study was aimed to establish the HPLC fingerprint of liposoluble components inDanshen capsule for quality evaluation. HPLC was run on a Welch ultimate XB-C18 column (250 mm × 4.6 mm, 5 μm) with acetonitrile-water as mobile phase in gradient elution at a flow rate of 1 mL·min-1. The column temperature was 25℃. The detection wavelength was 270 nm. The injection volume was 10μL. The results showed that 7 and 11 common peaks were selected as the HPLC fingerprint of liposoluble components inDanshen capsule from two manufactures, respectively. The similarities of 20 batches of samples were above 0.9. It was concluded that the analysis was stable and reproducible, which can be used as a basis for evaluating the quality control of liposoluble components in Danshen capsule.

Objective To establish a HPLC method for simultaneous determination of seven active components in Fufang Danshen tablets and Fufang Danshen dripping pills. Methods These seven compounds were analyzed simultaneously with a Zorbax C18 column by gradient elution using acetonitrile-0. 1% phosphoric acid solution as mobile phase, the flow rate was 1 mL·min-1 and the detection wavelength was set at 203, 270 and 281 nm, respectively. Results All the seven components showed good linear relation between peak area and concentration of the test, and the average recoveries were between 95. 1%-100. 4%. Tanshinone ⅡA was not detected in samples of dropping pills. Conclusion The HPLC method to determine the components including tanshinone ⅡA, salvianolic acid B, propanoid acid, protocatechuic aldehyde, notoginsenoside R1 , ginsenoside Rg1 and ginsenoside Rb1 of the two different Danshen preparations has been established, and it has the advantages of simplicity, high precision, good repeatability, and can be used for the quality control of two kinds of Fufang Danshen preparations. The content of tanshinone Ⅱ A in Fufang Danshen tablet was distinctly higher than that of dropping pills.

Objective To summanrize the operative method and follow-up data of total aortic arch replacement combined with transaortic stented graft implantation into the descending aorta (Sun's procedure) for acute Stanford type A aortic dissection.Methods Between August 2004 and March 2012,73 patients with acute type A aortic dissection underwent this procedure.60 males and 13 females ranging in age from 26 to 79 years (mean age,49,6 years).Right axillary or femoral artery cannulation was routinely used for cardiopulmonary bypass.Cerebral protection was achieved by bilatero-antegrade or selected hrain perfusion.The stented elephant trunk was implanted throuugh the aortic arch under hypothermic circulatory arrest.The stented elephant trunk was a 10cmlong self expandable graft.Patent false lumina were evaluated using computed tomography 3 months and once each year after discharge to evaluate the postoperative time course of the residual false lumen.Results Mean cardiopulmonary bypass time was (248.1±69.8)min,and selected cerebral perfusion time was (38.2±10.5)min.Hospital morality was 6.85 ％ (5/73).Thrombus obliteration of the residual false lumen in the descending thoracic aorta was observed in 9 1.7％ of the aortic dissections 3 months postoperatively.The mean follow-up time was(36.4 ± 31.6)months (range,2 to91 months).Survival at 1,5,7 years was 97％,87％ and 81％,respectively.Conclusion Total aortic arch replacement combined with transaortic stented paft implantation into the descending aorta is an effective treatment and n more promising choice for acute type A aortic dissection.

It is well known that puerarin possesses protective activity on neurodegenerative diseases. However, the exact path way involved in the protective effect of puerarin on MPP+ -induced cell death is unclear. In this study, we focused on mitochondria im pairment in the apoptotic process of MPP+ -elicited SH-SY5Y cells and detected the protection of puerarin. As evidenced by Trypan blue assay, the cell viability was significantly decreased by 1 mmol x L(-1) MPP+, but reversed by different concentrations puerarin pre treatment. Flow cytometer analysis revealed that MPP+ -induced SH-SY5Y cells apoptosis and arrested the cells in G2/M phase, where as puerarin pretreatment concentration dependently reversed the apoptosis ratio. In addition to the apoptosis ratio, 50.0 micromol x L(-1) puerarin pretreatment even altered the MPP+ -induced G2/M phase arrest. JC-1 assay suggested that MPP+ significantly opened MMP of the SH-SYSY cells; pretreatment with puerarin attenuated the deterioration of the MMP. Both ELISA and Western blotting showed that puerarin prevented the release of cytochrome c from the mitochondrial interior to the cystol elicited by MPP+. DNA ladder showed that typical DNA ladder was present in the MPP+ -induced SH-SY5Y cells. Additionally, MPP+ enhanced caspase-9 and caspase-3 ac tivity, respectively, while not caspase-8. However,the enhancement was concentration dependently blocked by puerarin pretreatment. Taken together, puerarin can modulate mitochondrial membrane potential and inhibit the cytochrome c releasing-caspase cascade to pre vent MPP+ -induced cell injury.
1-Methyl-4-phenylpyridinium ; pharmacology ; Apoptosis ; drug effects ; Blotting, Western ; Caspase 3 ; metabolism ; Caspase 8 ; metabolism ; Caspase 9 ; metabolism ; Cell Cycle ; drug effects ; Cell Differentiation ; drug effects ; Cell Line, Tumor ; Enzyme-Linked Immunosorbent Assay ; Flow Cytometry ; Humans ; Isoflavones ; pharmacology ; Membrane Potential, Mitochondrial ; drug effects ; Mitochondria ; drug effects

Asthma is a common chronic airway inflammatory disease in children.Currently, symptomatic control can be achieved in the majority of patients through a combination of β 2 receptor agonists for rapid relief of symptoms and inhaled corticosteroids for long-term control.As the only causal treatment modality at present, allergen-specific immunotherapy (AIT) may modify the natural course of asthma, and can control the symptoms, reduce airway hyperresponsiveness and improve lung function.In order to provide evidence for improving the effect of AIT on asthma, the mechanism of AIT in asthma and its effect on lung function were discussed in this paper.

OBJECTIVETo compare the effect aortic valve replacement(AVR) combined with aortic root enlargement and simple St.Jude Regent AVR in small aortic annulus patients.

METHODSFrom June 2008 to June 2012, 62 severe aortic valvular stenosis patients with small aortic annulus (annulus diameter of 15-21 mm) entered the study. Twenty-seven cases received AVR combined with aortic root enlargement (enlargement group) and 35 cases received simple St.Jude Regent AVR(non-enlargement group), 17 mm St.Jude Regent in 15 cases(17 mm group) and 19 mm in 20 cases (19 mm group). Aortic root enlargement techniques included Nicks in 2, modified Nicks in 6 cases, modified Manouguian in 19 cases. Patients were followed up and received ultrasonic cardiogram (UCG) 3, 12 months postoperatively and t-test was used for statistical comparison.

RESULTSIn enlargement group, 1 Nicks patient received reoperation due to aortic root hemorrhage, and died of mediastinal infection, 1 Manouguian patient received permanent pacemaker. In non-enlargement group, low cardiac output syndrome in 1 case. Three months and 12 months postoperative UCG showed, comparing to preoperation, effective orifice area (EOAI) increased significantly, postoperative transvalular pressure gradient and flow rate decreased significantly in each group (P = 0.000). Left ventricular diastolic diameter (LVDd) decreased significantly in both enlargement group and 19 mm group(P = 0.000), but no significant change in 17 mm group (P > 0.05). In non-enlargement group, 19 mm compared to 17 mm group, 3 months and 12 months postoperative EOAI increased significantly, pressure gradient, flow rate and LVDd decreased significantly(t = 2.449-12.291, P = 0.000-0.029). Comparing to enlargement group, there were significant differences in EOAI, pressure gradient, flow rate and LVDd in 17 mm group (t = 2.278-17.860, P = 0.000-0.028), but no significant differences in 19 mm group(t = 0.118-1.630, P = 0.110-0.907).

CONCLUSIONSFor small aortic annulus AVR patient, 19 mm and larger St.Jude Regent prosthetic valves may produce satisfied hemodynamic, otherwise, aortic root enlargement is recommended.

Adult ; Aged ; Aortic Valve ; surgery ; Female ; Follow-Up Studies ; Heart Valve Prosthesis ; Heart Valve Prosthesis Implantation ; methods ; Humans ; Male ; Middle Aged

Objective    To explore the operability of concomitant ablation for the patients with valvular heart diseases with left atrium bigger than 60 mm. Methods    We prospectively included 306 patients with concomitant ablation in our hospital between 2013 and 2015 year. Based on diameter of left atrium measured by intra-operative transesophageal echocardiography (TEE), we separated these patients into two groups including a group L (left atrium >60 mm, 93 patients, 55 males and 38 females at age of 57.0±10.1 years) and a group S (left atrium <60 mm, 213 patients, 120 males and 93 females at age of 55.2±9.9 years) and followed them on 4 time points (time on discharge, three months, six months, and one year after surgery). Then, we analyzed the impact of left atrial size on cardioversion outcome of surgical ablation based on the following data. Results    The successful rate of the group S and the group L in the 4 time points was 72.8% vs. 75.3%, 74.2% vs. 75.3%, 78.9% vs. 77.4%, and 77.0% vs. 77.4%, respectively . The result of both univariate logistic regression analysis and receiver operation characteristic(ROC) curve analysis showed that there was no statistical difference in cardioversion rates between the group S and the group L. And there was no evident correlation between size of left atrium and ablation failure. Conclusion    Patients with left atrium enlarged from 60 mm to 70 mm can achieve the same satisfactory results in cardioversion, and should not be the contraindication of concomitant surgical ablation.

ObjectiveTo explore the mechanism of Qigesan （QGS） in intervening in the migration and invasion of esophageal carcinoma TE-1 cells. MethodMicroarray technology was used to screen differentially expressed genes （DEGs） in the normal group and the QGS group， and the ontological functions and signaling pathways of DEGs were analyzed. The thiazolyl tetrazolium （MTT） assay was used to detect the effect of QGS on the viability of TE-1 cells. In the subsequent experiments for verification， a blank group， a transforming growth factor-β₁ （TGF-β₁） group， a TGF-β₁ + QGS group， and a TGF-β₁ + SB431542 group were set up. The cell morphology in each experimental group was observed by microscopy. The migration and invasion abilities of cells were detected by wound healing assay， and the mRNA expression levels of E-Cadherin， vimentin， Smad2， and Smad7 were detected by Real-time quantitative polymerase chain reaction （Real-time PCR）. The protein expression of E-Cadherin， vimentin， p-Smad2/3， Smad2/3， and Smad7 was detected by Western blot. ResultThere were 1 487 DEGs between the QGS group and the blank group， including 1 080 down-regulated ones （accounting for 72.63%） and 407 up-regulated ones. The down-regulated genes were mainly involved in biological processes such as cytoskeletal protein binding， ATP binding， adenylate nucleotide binding， and adenylate ribonucleotide binding， and the involved Kyoto Encyclopedia of Genes and Genomes （KEGG） pathways included TGF-β signaling pathway， cell cycle， extracellular matrix-receptor interaction protein， tumor pathways， and oocyte meiosis. The up-regulated genes were mainly involved in RNA binding， DNA binding， transcriptional regulator activity， transcriptional activator activity， and nucleotide binding， and the KEGG pathways involved mainly included mitogen-activated protein kinase （MAPK） signaling pathway， bladder cancer， renal cell carcinoma， cancer pathways， and p53 signaling pathway. Compared with the blank group， the inhibition rate of cell viability of TE-1 cells increased after QGS （20， 30， 40， 60， 80 mg·L^-1） intervention for 12， 24， 36， 48， 60 h （P<0.05）， and the inhibition rate was time- and dose-dependent. Compared with the blank group， the TGF-β₁ group showed lengthened cells with fibroblast phenotype. Compared with the TGF-β₁ group， the TGF-β₁ + QGS group showed shortened cells with normal morphology and epithelial phenotype. The cell morphology in the TGF-β₁ + SB431542 group was similar to that of the TGF-β₁ + QGS group. Compared with the blank group， the TGF-β₁ group showed potentiated ability of cell migration and invasion （P<0.05）. Compared with the TGF-β₁ group， the TGF-β₁ + QGS group and the TGF-β₁ + SB431542 group showed inhibited and weakened migration and invasion abilities of cells （P<0.05）. However， there was no significant difference in migration and invasion abilities between the TGF-β₁ + QGS group and the TGF-β₁ + SB431542 group. The mRNA expression levels of vimentin and Smad2 in the TGF-β₁ group were higher （P<0.05）， and the mRNA expression levels of E-Cadherin and Smad7 were lower （P<0.05） than those in the blank group. Compared with the TGF-β₁ group， the TGF-β₁ + QGS group and the TGF-β₁+ SB431542 group exhibited decreased expression levels of vimentin and Smad2 mRNA （P<0.05）， and elevated expression levels of E-Cadherin and Smad7 mRNA （P<0.05）. Compared with the blank group， the TGF-β₁ group showed up-regulated protein expression levels of vimentin， p-Smad2/3， and Smad2/3 （P<0.05）， and reduced protein expression levels of E-Cadherin and Smad7 （P<0.05）. Compared with the TGF-β₁ group， the TGF-β₁ + QGS group and the TGF-β₁ + SB431542 group displayed decreased protein expression levels of vimentin， p-Smad2/3， and Smad2/3 （P<0.05）， and increased protein expression levels of E-Cadherin and Smad7 （P<0.05）. ConclusionThe ethyl acetate extract of QGS inhibits the epithelial-mesenchymal transition （EMT） of TE-1 cells through the TGF-β₁ pathway to reduce the migration and invasion of TE-1 cells.

ObjectiveTo investigate the mechanism of icariin in ameliorating efferocytosis dysfunction and inflammatory response of alveolar macrophages induced by cigarette smoke extract via the peroxisome proliferator-activated receptor gamma （PPARγ） signaling pathway. MethodThe untreated rat alveolar macrophages （NR8383） were taken as the blank group. The NR8383 cells treated with 10% cigarette smoke extract were divided into model， low-， medium-， and high-dose （10， 20， 40 μmol·L^-1） icariin， PPARγ inhibitor， and PPARγ inhibitor + low-， medium-， and high-dose icariin groups. Alamar blue colorimetry was employed to examine the proliferation and toxicity of icariin on NR8383 cells. The efferocytosis rate of NR8383 cells was detected by flow cytometry. Enzyme-linked immunosorbent assay was employed to measure the levels of tumor necrosis factor-alpha （TNF-α）， transforming growth factor-β₁ （TGF-β₁）， and milk fat globule-epidermal growth factor 8 （MFG-E8）. Western blot and Real-time fluorescence quantitative polymerase chain reaction （Real-time PCR） were employed to determine the protein and mRNA levels， respectively， of PPARγ， CD36， and RAS-related C3 botulinum toxin substrate 1 （Rac1）. ResultThe efferocytosis dysfunction model of NR8383 was established with the cigarette smoke extract. Compared with the blank control group， the model group showed decreased efferocytosis rate （P<0.05）， elevated TNF-α level （P<0.05）， lowered TGF-β₁ and MFG-E8 levels （P<0.01）， and down-regulated mRNA and protein levels of PPARγ， CD36， and Rac1 （P<0.05， P<0.01）. Compared with the model group， the treatment with icariin increased the efferocytosis rate （P<0.05， P<0.01）， lowered the TNF-α level （P<0.01）， elevated TGF-β₁ and MFG-E8 levels （P<0.05）， and up-regulated the protein and mRNA levels of PPARγ， CD36， and Rac1 （P<0.05， P<0.01）. Compared with icariin alone， PPARγ inhibitor + icariin decreased the efferocytosis rate （P<0.05） and down-regulated the protein and mRNA levels of PPARγ （P<0.05， P<0.01）. In addition， PPARγ inhibitor + low-dose icariin down-regulated the protein level of CD36 （P<0.01） and PPARγ inhibitor + low-/medium-dose icariin up-regulated the protein level of Rac1 （P<0.05）. ConclusionIcariin ameliorates the cigarette smoke extract-induced efferocytosis dysfunction of alveolar macrophage by regulating the PPARγ signaling pathway and cytoskeletal structure rearrangement.