Table of Content

    05 October 2014, Volume 34 Issue 10
    MiR-124a accelerates pancreatic progenitor cells differentiation of mesenchymal stem cells from human placental through TGF-β pathway
    2014, 34(10):  1309-1314. 
    Asbtract ( 825 )   PDF (1464KB) ( 868 )  
    Related Articles | Metrics
    Objective The aim of this study is to improve the potential of pancreatic progenitor cells differentiation of human placenta derived mesenchymal stem cells (PMSCs) by miR-124a mediates post-transcriptional regulation of its mRNA targets TGFBR1 and BMPR1B . Methods We used lentiviral vectors to stably and specifically over express miR-124a and inhibited the miR-124a function by its antagomir. In addition, we analyzed the relationship between miR-124a and target genes expression. Real-time PCR, Western blot and immunofluorescent staining were used to test the mRNA and protein expression variation and assess the ability of PMSCs to differentiate into pancreatic progenitor cells. Results Overexpression of miR-124a led to repression of endogenous TGFBR1 and BMPR1B, and inhibition of miR-124a relieved the repression of TGFBR1 and BMPR1B. Overexpression of miR-124a in PMSCs resulted in up-regulated of pancreatic-specific genes (Ngn3, Nkx6.1, PDX-1 and Insulin) (P<0.05)and increased proportions of Insulin and PDX-1 positive events compared to control treated cells. Conclusion miR-124a is involved in pancreatic progenitor cells differentiation of PMSCs partially via suppression of the TGFBR1 and BMPR1B genes. Furthermore, the miR-124a accelerates pancreatic progenitor cells differentiation, possibly mediated by TGF β pathway.
    Toll-like receptor activation and stimulation promote the secretion of matrix metalloproteinases 9 of human ovarian cancer via co-cultrued with tumor associated macrophage
    2014, 34(10):  1315-1320. 
    Asbtract ( 733 )   PDF (1096KB) ( 652 )  
    Related Articles | Metrics
    Objective To investigate the influence of M2-type macrophage on expression of matrix metalloproteinase 9(MMP-9) in ovarian cancer cell, and to analyze the underlying mechanism about Toll-like receptors signaling pathway. Methods 320nM PMA was added to induce THP-1 cell into M2-type macrophage in vitro. M2-type macrophage and SKOV3 non-contacting co-culture model was established by Transwell method. After the co-cultrue process of 12 and 24 h, TLR1, 2, 6 and MMP-9 mRNA were detected by Real-time PCR. MyD88, TRAF6, and P-NF-κB and MMP-9 expression level were evaluated by Western blot. Testing the expression of MMP-9 after SKOV3 was stimulated with TLR1, 2 and 6 agonist for the time of 6, 12 and 24 h respectively. Results Type M2 macrophages could be induced differentiation by PMA. After the co-culture process of 24 and 48 h, MMP-9 mRNA and protein relative expressions in SKOV3 cells were significantly higher (P<0.05). The content of TLR1, 2 and 6 mRNA was highly expressed in SKOV3 (P<0.05). Co-cultured after 24 and 48 h, TLRs signaling pathway proteins MyD88, TRAF6, and P-NF-κB have synchronous increased expression in SKOV3(P<0.05). TLR1, 2 and 6 agonist respectively stimulated SKOV3 for 6 h, 12 h, 24, MMP-9 mRNA level had a significantly high expression (P<0.05). Conclusion Polarization-type tumor-associated macrophage could promote MMP-9 expression in ovarian cancer cells, and its mechanism is possibly though stimulating and activation of TLRs signaling pathway, which is closely connected with invasion and metastasis of ovarian cancer.
    Inhibitory effect of telmisartan on non-alcoholic fatty liver fibrosis in rats
    2014, 34(10):  1321-1326. 
    Asbtract ( 613 )   PDF (1503KB) ( 631 )  
    Related Articles | Metrics
    Objective To study the inhibited effect of telmisartan (Tel) on non-alcoholic fatty liver fibrosis (NLFLF) in rats. Methods Sixty Wistar rats were randomly and equally divided into 6 groups. Two groups of them supplied with choline-supplemented L-amino acid-defined diet(CSAA) : CSAA group fed with CSAA diet only, CSAA treatment group fed with CSAA diet and supplemented with Tel of 2.5 mg/(kg BW?d)(CSAA+Tel-high). The residual four groups fed with choline-deficient L-amino acid-defined (CDAA) diet and supplemented with Tel of 0(CDAA), 0.5 (CDAA+Tel-low), 1.0(CDAA+Tel-med) and 2.5(CDAA+Tel-high) mg/(kg BW?d). The total experimental period was 10 weeks. Serum biological parameters were determined routinely. Expression of α-smooth muscle actin (α-SMA) and transforming growth factor-β1 (TGF-β1) in liver tissue were determined by immunohistochemistry, and pathological changes in liver tissues were detected by Azan staining. The messenger RNA (mRNA) expressions of type I procollagen, matrix metalloproteinases (MMPs) and tissue inhibitor of metalloproteinase (TIMPs) were evaluated using real-time quantitative PCR. Results The levels of hyaluronic acid, alkaline phosphatase, γ-gluamyl transpeptidase and total bilirubin in serum of CDAA group were all higher than those of CDAA diet supplemented with Tel (P <0.05 or P<0.01). The quantity of α-SMA and TGF-β1 was higher in CDAA rats compared with Tel treated rats(P<0.01). The mRNA of type I procollagen was higher than that of the Tel treated rats(P<0.01), and that decreasing as the dose of Tel increasing; on the same time, the expression of MMP13 increased, while the expression of MMP2,9 and TIMP1,2 decreased. Tel also controlled the CDAA diet rats body weight gain. Conclusions Tel suppressed NLFLF in rats through inhibited HSCs activation, it may become a promising medicine to control non-alcoholic fatty liver disease.
    Effect of adenovirus-mediated PML (NLS-) over-expression on the proliferation and apoptosis of NB4 leukemic cells
    2014, 34(10):  1327-1332. 
    Asbtract ( 846 )   PDF (1431KB) ( 598 )  
    Related Articles | Metrics
    Objective To investigate the effect of PML (NLS-) on proliferation and apoptosis of leukemic NB4 cells by the over-expression of PML(NLS-) induced by adenoviruses. Methods Recombinant adenovirus plasmid Ad-PML (NLS-) was digested and linearized with Pac I enzyme then transfected into AD293 cells. After amplified the Recombinant adenovirus Ad-PML(NLS-) for four times, to test recombinant adenovirus titer. After Recombinant adenovirus transfected into NB4 cells, infection efficiency was detected by fluorescence microscopy imaging and flow cytometry, the transcription and expression level of PML(NLS-) in NB4 cells were detected by RT-PCR and Western blot. Cell proliferation was detected by MTT. Cell cycle and apoptosis was detected by flow cytometry. Results Recombinant adenovirus plasmid Ad-PML (NLS-) was exactly digested and sequenced. The titer of amplified virus was . The efficiency of transfection was 75%, and PML(NLS-) had a high level expression in NB4 cells. The activity of cell proliferation in NB4 cells was significant enhanced compared with the untransfected and empty viral vector (p<0.05). The proportion of cells in S phase was obviously increased while which was obviously decreased in G1 phase. The rate of apoptosis in the experimental group was obviously lower than the empty viral vector. Conclusions The over-expression of PML(NLS-) could promote the proliferation of NB4 cells in vitro and inhibit the apoptosis.
    Combinating COX multivariate analysis with ROC curve to evaluate the prognostic value of DNA Repair gene in Nasopharyneal Carcinoma
    2014, 34(10):  1333-1338. 
    Asbtract ( 1251 )   PDF (952KB) ( 528 )  
    Related Articles | Metrics
    Objective Using COX multivariate analysis and ROC curve to evaluate the prognostic value of DNA repair gene in patients with Nasopharyngeal carcinoma. Methods Between May 2007 and February 2012, all 100 untreated patients with NPC, who were planned to receive IMRT at the People's Hospital of Guangxi Autonomous Region were enrolled in this study. Screening for more than 1 year follow-up of 71 cases, formalin-fixed tumor biopsy specimens from 71 untreated patients with NPC were analyzed by immunohistochemical methods. Spearman's analysis was put into use in the correlation of DNA-PKcs and BRCA1 expression levels and clinical characteristics. Kaplan-Meier survival curves analyzed the relationship between expression of DNA-PKcs and BRCA1 and prognostic groups which were established by ROC curves. And Cox proportional hazards regression multi-factor survival analysis was carried out on the prognosis at last. Results 1) There was a significant positive correlation between the expression level of DNA-PKcs and survival time of patients(P<0.05). 2) Moreover, patients with high DNA-PKcs expression had significantly better survival than patients with low levels of DNA-PKcs(P<0.01). 3) On multivariate analysis, only DNA-PKcs expression level is an independent prognostic factor(P<0.01). No significant association was found between the level of BRCA1 expression and the clinical outcome. Conclusions DNA-PKcs expression level was an independent factor in prognostic and the patients with high level had a better survival.
    Atorvastatin inhibits the proliferation and ptomotes apoptosis of VSMC by the transcription factor AP1 in rats
    2014, 34(10):  1339-1343. 
    Asbtract ( 525 )   PDF (1475KB) ( 524 )  
    Related Articles | Metrics
    Objective To investigate atorvastatin inhibits the proliferation and ptomotes apoptosis of VSMC bythe transcription factor AP1 in rats.Methods 80 rats were randomly divided into four groups: normal group,AS group, high-dose atorvastatin group (40mg/kg?d), low-dose atorvastatin group (10mg/kg?d).The VSMC apoptosis was detected by TUNEL assay.The protein expression level of AP1 andα-SM-actin were measured by immunohistochemical analysis and western blotting. Results TG、TC and LDL were significantly decreased in two atorvastatin groups (P<0.05). Atorvastatin significantly inhibited the VSMC proliferation and induced apoptosis (P<0.05). Atorvastatin regulated AP1 andα-SM-actin protein expression was significantly decreased(P<0.05).Conclusions Our results showed that the atorvastatin suppresses proliferation and promote apoptosis of VSMC through down-regulation of AP1 expression in rats.
    The Effect of PPAR-γ Ligand on Proliferation and Secretion and Invasion of JEG-3 Choriocarnoma Cells inVitro
    2014, 34(10):  1344-1347. 
    Asbtract ( 100 )   PDF (606KB) ( 485 )  
    Related Articles | Metrics
    Objective To observe the effect of ligand of peroxisome proliferators-activated receptor gamma (PPAR gamma) on the proliferation and secretion of trophoblast and choriocarnoma cells (JEG-3) and to study the role played by PPAR gamma during the process of JEG-3 activation. Methods We employed MTT assay observing the growth of the cells and IEMA observing the secretion of hcG in the cells. Matrigel invision chambers were performed to analyse the cell migration and invasion.Results The proliferation of JEG-3 was suppressed by PGZ with a low dose-dependent manner . The numbers of JEG-3 was obviously inhibited by PGZ(p<0.01)with increasing concentration.Conclusion The results obtained with this in vitro system demonstrated that PPARgamma activation could inhibit JEG-3 proliferation and invasiveness. PPARgamma may be considered as a new therapeutic target for gestational trophoblastic tumor in humans.
    Body mass index is associated with hypertension and blood lipid in mongolian people of inner mongolia pastoral areas
    2014, 34(10):  1348-1351. 
    Asbtract ( 186 )   PDF (509KB) ( 644 )  
    Related Articles | Metrics
    Objective To investigate correlation between body mass index with hypertension and blood lipid of Mongolian people in inner Mongolia pastoral areas. Methods Investigation and analysis of the relationship between body mass index with hypertension and blood lipid to the 951 Mongolian people who are over the age of 18. Results Overweight and obesity was higher males than females in Mongolia population (P <0.01), Hypertension, lipid abnormality prevalence increases with an increase body mass index. Overweight and obesity people with hypertension, lipid abnormality prevalence was significantly higher than the normal group (P <0.01). Body mass index was associated positively with Hypertension, lipid abnormality prevalence. Conclusions Body mass index is a risk factor for hypertension and lipid abnormality prevalence to Mongolian people, Control body weight can prevent and reduce the occurrence of chronic diseases.
    Overexpression of MIPU1 reduce Doxorubicin-induced apoptosis in human embryonic kidney 293 Cells
    2014, 34(10):  1352-1357. 
    Asbtract ( 87 )   PDF (1542KB) ( 501 )  
    Related Articles | Metrics
    Objective To explore the affection of overexpression MIPU1 on DOX-mediated apoptosis and the mechanisms underlying, we hope that our studies would provide novel insight into the biological functions of Mipu1, and provide a new clue for preventing the side-effects of DOX during anticancer implication. Methods Apoptosis was induced by Doxorubicin in this experiment. The eukaryotic expression plasmid pEGFP-MIPU1 was constructed previously and delivered into the cells to increase the expression of MIPU1. Firstly, MTT assay was used to estimate the cells viability. Then apoptosis was assessed by using Hoechst staining and flow cytometry (FCM). Thirdly, Western blot and RT-PCR were performed to detect the expression of Bax, P53 and Bcl-2 at the mRNA and protein levels respectively. Results After transfected with pEGFP-MIPU1, the overexpression of MIPU1 significantly attenuated the mortality rate induced by DOX (P<0.05 VS pEGFP+DOX), and markedly decreased the cellular apoptosis treated with DOX (P<0.01 VS pEGFP+DOX ); The overexpression MIPU1 inhibited the increase of P53 and Bax induced by DOX (P<0.05 VS pEGFP+DOX), while reversed the decrease of Bcl-2 expression in DOX-induced HEK293 cells (P<0.05 VS pEGFP+DOX). Conclution Overexpression MIPU1 inhibited apoptosis in HEK293 cells induced by DOX, and the possible mechanism is that MIPU1 decreased the expression of P53 and Bax, and promoted the expression of Bcl-2 in DOX-induced HEK293 cells.
    Heme Oxygenase-1 can alleviate the oxidative damage caused by serum of smoking rats on human umbilical vein endothelial cell
    2014, 34(10):  1358-1362. 
    Asbtract ( 80 )   PDF (1010KB) ( 403 )  
    Related Articles | Metrics
    Objective To study whether Heme Oxygenase-1(HO-1) can alleviate the oxidative damage caused by serum of smoking rats on human umbilical vein endothelial cell(HUVEC). Methods Fifteen male Sprague-Dawley rats were randomized into control group,smoking group,and smoking with Zincprotoporphyrin(ZnPP) group.Western blot was used to detect the expression of HO-1 in carotid arteries of the rats.Also the expression of HO-1was detected in HUVEC cultured in the serum of normal rats,smoking rats and smoking with ZnPP rats.The reactive oxygen species were detected in HO-1-overexpressing and HO-1-lowexpressing HUVEC ,cultured in the serum of smoking rats.Results The expression of HO-1 in carotid arteries of smoking rats was significantly higher than that of normal rats(P <0.01).Both the serum of smoking rats and HO-1depressed smoking rats could induced the expression of HO-1 in HUVEC,and the role of the latter was more obvious(P <0.01).The reactive oxygen species of HUVEC cultured in the serum of smoking rats were more than that cultured in the serum of nornal rats(P<0.01),also the HO-1 could release the oxidative damage(P<0.01).Conclusion Smoking can cause the oxidative damage to HUVEC ,and HO-1 can alleviate the damage.
    Hepatitis C virus (HCV) 5′ non-coding region (NCR) gene-specific LNAzyme significantly inhibits HCV replication and expression in vitro
    2014, 34(10):  1363-1366. 
    Asbtract ( 76 )   PDF (623KB) ( 534 )  
    Related Articles | Metrics
    Objective To investigate the inhibitory effects of LNAzyme targeting the hepatitis C virus(HCV) 5′ non-coding region internal ribosome entry site(IRES) on HCV RNA replication and expression in cells. Methods The sequence encoding DNAzyme, thiolmodificated DNAzyme and LNAzyme targeting against the HCV IRES(located in the 5′ non-coding region) were designed and synthesized. The following experimental groups were set up: DNAzyme group, S-DNAzyme group, LNAzyme group, blank control group, empty liposomes group, random-LNAzyme group, and transfected by cationic liposomes into HepG2.9706 cells. The level of HCV RNA and luciferase gene expression of supernatant was tested by real-time fluorescent quantitative PCR and chemiluminescence technique at 24, 48 and 96 hours after treatment. LNAzyme’s cyto-toxicity on cell was evaluated by MTT method. Results Significant down-regulation of HCV RNA replication and luciferase gene expression was noted in the LNAzyme group when compared with other groups (all P<0.05). The average inhibition rates were 48.02% and 53.05%, respectively, and with the treatment time prolonged, the inhibition rate was increasing, 96 hours later, the average inhibition rates were 81.21% and 84.25%, respectively. There’s no obvious toxicity on cell. Conclusion LNAzyme has a significant inhibitory effect on HCV RNA replication and expression in vitrol, and was stronger than the thiolmodificated DNAzyme.
    LPS Up-regulates HIF-1? and GLUT Expressions in Rats
    2014, 34(10):  1367-1371. 
    Asbtract ( 110 )   PDF (898KB) ( 464 )  
    Related Articles | Metrics
    Objective Characterization of glucose transporter (GLUT) family and potential role of HIF-1? in lipopolysacchride (LPS)-induced endotoxemic rats was investigated, and this information helps to understand GLUT family in endotoxemic rats. Methods SD rats were treated with a single dose injection (i.p.) of LPS (2 mg/kg), and rats in control group were given equal amount of NaCl (0.9%) (n=6). The body temperature was detected after LPS treatment for 0 ~ 24 h. IL-1? release was evaluated by ELISA assay. GLUT mRNA expression was determined by RT-PCT assay. HIF-1? and GLUT1 protein expression were examined. Results LPS increased rats’ body temperature and IL-1? release in serum(P<0.05). GLUT1 and GLUT4 expressed in brain, heart and liver. GLUT2 expressed in brain and liver. GLUT3 mainly expressed in brain. LPS increased GLUT1 mRNA and protein expression in the brain (P<0.01). HIF-1? kept stability in the brain of LPS-challenged rats (P<0.001). Conclusion LPS induced GLUT1 overexpression and HIF-1? stability in the brain of the endotoxemic rats. It indicated that HIF-1?-induced GLUT1 upregulation might be a potential way to regulate glucose metabolism in LPS-challenged rats.
    DR2 attenuates myocardial ischemia/reperfusion injury of rats in vitro
    2014, 34(10):  1372-1375. 
    Asbtract ( 83 )   PDF (777KB) ( 475 )  
    Related Articles | Metrics
    Objective To observe the effects of dopamine receptors-2 (DR2) on the myocardial ischemia/reperfusion (I/R) injury in rats and to study the possible mechanisms. Methods 40 Wistar rats were randomly divided into 4 groups (n=10): control group, I/R group, Bromocriptine group (Bro) and Haloperidol group (Hal). Myocardial ischemia/reperfusion injury of isolated rats was induced with Langendorff system; The heart function was recored by Powerlab; LDH, CK activities of coronary effluent and SOD activity and MDA content of myocardial tissue homogenate were measured by colorimetric method; Myocardial cell apoptosis was detected by TUNEL staining; The expression of DR2, Bcl-2, caspase-3 and caspase-9 was detected by Western blot. Results Compared with control group, the expressions of DR2, Bcl-2, caspase-3, caspase-9, the activity of LDH and CK, the MDA content, the rate of cell apoptosis were increased (P<0.01), but the SOD activity and heart function were decreased in the I/R group (P<0.01). Compared with I/R group, Bro decreased the activity of LDH and CK, the MDA content, the rate of cell apoptosis, the expression of caspase-3 and caspase-9, increased the SOD activity and Bcl-2 expressions, improved heart function (P<0.01). Hal did not change the above indexes. Conclusion Our results suggest that DR2 inhibites I/R injury through antioxidation, scavenging free radical, up-regulation of Bcl-2 expressions and down-regulation of caspase-3 and caspase-9 expressions.
    PTTG1 Induces Migration And Invasion Of Non-small Cell Lung Cancer Through Epithelial-mesenchymal Transition
    2014, 34(10):  1376-1380. 
    Asbtract ( 75 )   PDF (1135KB) ( 418 )  
    Related Articles | Metrics
    Objective To investigate the role of PTTG1 in the migration and invasion of Non-small cell lung cancer. Methods To detect the expression of PTTG1, E-cadherin and Vimentin in 80 cases of NSCLC using immunohistochemistry. Cells were divided by four groups : ①A549/con, cells were transfected by empty vector②A549/PTTG1, cells were transfected by purpose gene ③Scr/H1299, cells were transfected by empty vector ④SiPTTG1/H1299, cells were knocked down purpose gene. Western blot was used to analyze the expression of PTTG1, E-cadherin and Vimentin. Results The protein expression of PTTG1 in NSCLC was negatively correlated with E-cadherin and positively correlated with Vimentin (P<0.05). H1299 cells expressed higher PTTG1, and A549 cells expressed lower PTTG1. The expressions of PTTG1 and Vimentin were lower in SiPTTG1/H1299 cells than those in Scr/H1299 and H1299 cells after trancfected 24 hours, but the E-cadherin expression was higher. At the same time, the protein expression of Vimentin was up-regulated and the expression of E-cadherin was down-regulated in A549/PTTG1 cells. Conclusions PTTG1 can promote migration and invasion of NSCLC through EMT.
    TBB inhibits the proliferation and migration of thyroid papillary carcinoma cell line FTC133 via WNT/β-CATENIN signaling pathway
    2014, 34(10):  1381-1385. 
    Asbtract ( 101 )   PDF (875KB) ( 490 )  
    Related Articles | Metrics
    Objective To observe the effects of 4,5,6,7-tetrabromobenzotriazole(TBB) on the expressions ofCK2ɑ,β-CATENIN and SURVIVINin thyroid papillary carcinoma cell line FTC133and to explore the possible underlyingmechanism. Methods FTC133 cellswere cultured in vitro and divided into control group(DMSO), TBBgroups(12.5, 25, 50μmol/L)randomly. The proliferationrateand migration of FTC133 cells was detected byMTTand wound healing method. TheCK2ɑ, β-CATENIN and SURVIVIN mRNA and protein expression levelswere determined by RT–PCR and Western blot. Results Compared with control group, the proliferationrate and migration of FTC133 cells wereinhibited by TBBin a dose–dependentmanner(P<0.01).The expression levels of mRNA and protein ofCK2ɑ were significantly decreased in the presence of different TBB in FTC133 cells(P<0.01), the protein expression level of β-CATENIN and SURVIVIN were decreased, too(P<0.01).Conclusion TBB inhibits the proliferation and migration of thyroid papillary carcinoma cell line FTC133 via WNT/β-CATENIN signaling pathway.
    Adiponectin alleviates high glucose induced vascular endothelial cells injury
    2014, 34(10):  1386-1390. 
    Asbtract ( 86 )   PDF (1366KB) ( 379 )  
    Related Articles | Metrics
    Objective: To observe the protective effect of adiponectin ( APN ) on high glucose induced vascular endothelial cell injury ,and investigate the expresstion of NF-κB and LOX-1 in the role of the protection process.Methods: D-Glucose of 30mmol/L effect on HUVEC-12 for 48 hours to make the model of injured vascular endothelial cells, adiponectin with different concentration (10,20,40μg/mL) for 48 hours and adiponectin of 20μg/mL for different time(12,24,48,72h)effected on the cell,inverted phase contrast microscope was used to observe the morphologic changes of the endothelial cells and the expression of NF-κB and LOX-1 protein in the HUVEC-12 was detected by Western Blotting, and NF-κB nuclear translocation in cells was observed by indirect immunofluorescence.Results: D-Glucose-induced HUVEC-12 were effected by adiponectin with different density and time, The morphologic changes of the cells converted to ameliorate: the reflected light of the HUVEC-12 was strengthened, particulate matter in cells tended to be not clear and the cell's shape converted from roundness to flat or polygon, NF-κB and LOX-1 protein expression were down-regulated partly with a dose and time-dependence(n=3,P<0.05).Conclusion: Adiponectin (APN) may down-regulate LOX-1 protein expression by NF-kB signaling pathway so as to have the protective effect on D-Glucose-induced HUVEC-12.
    The influence of ADAM33 to the expression of NF-κB and TGF-β1 in IL-4-stimulated human airway smooth muscle cells
    2014, 34(10):  1391-1396. 
    Asbtract ( 85 )   PDF (686KB) ( 523 )  
    Related Articles | Metrics
    Objective To investigate the influence of a disintegrin and matrix metalloprotease 33 (ADAM33) to the expression of nuclear factor-kappa B(NF-κB) and transforming growth factor-β1(TGF-β1) in interleukin-4 (IL-4)-stimulated human airway smooth muscle cells (HASMCs),and to provide a new theoretical basis for further improve the pathogenesis of asthma. Methods 50 μg/L IL-4 stimulated HASMCs for 24 hours, and the unstimulated cells were used as the control group, real-time quantitative PCR and Western blot were used to detect the expression of ADAM33.ADAM33-siRNA was transiently transfected into HASMCs after IL-4 stimulated HASMCs for 24 hours, real-time quantitative PCR and Western blot were respectively used to detect inhibition rates of ADAM33-siRNA and the expression of TGF-β1 and NF-κB at the mRNA level and the protein level. Results 50 μg/L IL-4 group was significantly promoting the expression of ADAM33 in HASMCs compared with the control group(P <0.05), the expression of ADAM33 at the mRNA level increased by approximately 4.36 times, and the protein level increased by approximately 3.3 times; ADAM33-siRNA-575 significantly inhibited the expression of ADAM33 in HASMCs;The relative expression of TGF-β1 mRNA in interference group, negative control group and blank control group were 0.602±0.024,1.01±0.176 and 1.239±0.171, respectively;the relative expression of NF-κB mRNA were 0.54±0.08,1.014±0.21 and 1.049±0.378,respectively; the relative expression of TGF-β1 protein were 0.227±0.016,0.7±0.048 and 0.715±0.025,and the relative expression of NF-κB protein were 0.335 ±0.048,0.922±0.04 and 0.943±0.046,respectively.Both at the mRNA level and the protein level, the expression of TGF-β1 and NF-κB in the interference group were significantly lower than those in the negative control group or in blank control group (P <0.05). Conclusions ADAM33 may be a key mediator in IL-4/NF-κB/TGF-β1 signaling pathway in HASMCs, and is expected to become an important target for prevention and treatment of asthma.
    Urinary incontinence development following laparoscopic radical prostatectomy
    2014, 34(10):  1397-1400. 
    Asbtract ( 149 )   PDF (469KB) ( 558 )  
    Related Articles | Metrics
    Objective To assay the time-variations and relating factors of Stress Urinary Incontinence (SUI) after radical prostatectomy. Methods During Mar.2010 to Nov.2013, 91 cases of laparoscopic radical prostatectomy were performed by a single surgeon, followed-up over 1 year. Basic information of all cases: the age range was 51~75 years, 67 on average; PSA range before surgery was 0.1~50.8 μg/L, 10.3 μg/L on median; the Gleason score was 6~8; and TNM stage range T1c~T2c. The catheter removal undertook 2 weeks after operation, then analyzed the incontinence rate and development pattern of incontinence after surgery. Urinary continence defined as 3 below conditions: urine leakage free, little leakage without urinal pads or less than 1 pad per day. Results the follow-up visit range 1~45 months, 18 on average. In line with the 3 definitions, urinary continence rate after catheter removal were: 0%, 5% and 33%; 30%, 63% and 93% by 3 months after surgery; 76%, 98% and 100% by 12 months after surgery. Conclusion the SUI after laparoscopic radical prostatectomy is a common, however, the majority of which can improve within 3~6 months after surgery, and reach basic control within 1 year.
    The protein expression of Notch and HES is crucial in the restenosis of vein graft in rat
    2014, 34(10):  1401-1404. 
    Asbtract ( 98 )   PDF (744KB) ( 514 )  
    Related Articles | Metrics
    Objective The result of the vein graft is poor as for restenosis. We want to investigate the effect of Notch signaling on restenosis of the vein graft. Methods Under the microscope rats were interposed the left jugular vein into the left common carotid artery, including control group, DAPT group and DMSO group. These data were measured including Media/Intima Ratio and PCNA. The expression level of Notch1 and HES1 protein was examined by Western blot. Result The protein level of Notch1 and HES1 were highly expressed in vascular smooth cells of vein graft. DAPT can inhibit the protein expression of both Notch1 and HES1 and the proliferation of vSMCs. Conclusion Notch signaling is crucial for restenosis of vein graft. The restenosis of vein graft is attenuated as the Notch signaling is inhibited.
    VEGF Promotes HUVEC Migration and Angiogenesis via up-Regulation of CCN2
    2014, 34(10):  1405-1409. 
    Asbtract ( 116 )   PDF (1074KB) ( 582 )  
    Related Articles | Metrics
    Objective: To explore the effect of VEGF-induced up-regulation of CCN2 in osteoblasts mediates biological behavior in human umbilical endothelial cells. Methods: Expression of CCN2-mRNA and CCN2-protein were examined in osteoblates in the presence of VEGF by Real time PCR and ELISA. Generation of osteoblast-conditioned supernatant. HUVECs were divided into three groups: Control group, OSE group, VEGF-OSE group (n=3). The chemically synthesized CCN2-siRNA was transfected into osteoblasts. The ability of cell migration was analyzed by the Transwell assay. The capability of cell to form capillary-like tubes in vitro was assessed on Matrigel assay. Results: VEGF increases the expression of CCN2 mRNA and protein in osteoblasts in a time- and dose-dependent manner. CCN2 promotes HUVEC migration and capillary tube-forming in vitro(P<0.05). These effects were prevented by an antibody against CCN2 or by small interfering RNA-mediated knockdown of osteoblast CCN2 (P<0.05). Conclusion: VEGF-induced up-regulation of CCN2 in osteoblasts mediates the ability of migration and angiogenesis in HUVEC.
    Expression of Bcl-2,Bax and caspase-9 in nasal polyps
    2014, 34(10):  1418-1419. 
    Asbtract ( 91 )   PDF (752KB) ( 476 )  
    Related Articles | Metrics
    Pathophysiology role of RhoA/ROCK signalling pathway in progression of atherosclerosis
    2014, 34(10):  1422-1425. 
    Asbtract ( 148 )   PDF (519KB) ( 889 )  
    Related Articles | Metrics
    RhoA/ROCK signaling pathway is ubiquitously involved in regulation of actin cytoskeleton and various cell behaviors, including cell contraction, adhesion, proliferation, gene expression, and so on. In the past few decades, accumulating experimental and clinical evidences suggest it plays an important role in atherosclerosis. Thus, revealing the molecular mechanisms and inhibition of RhoA/ROCK pathway will undoubtedly deepen our understanding of cardiovascular disease and even maybe a promising therapeutic target.
    A discussion on government responsibility of Primary healthcare
    2014, 34(10):  1426-1429. 
    Asbtract ( 85 )   PDF (612KB) ( 598 )  
    Related Articles | Metrics
    What role the government should play in the primary healthcare system, undertake what kind of responsibility, and why? These are focus in the process of the primary healthcare system legislation. The paper based on the definition of the meaning of government responsibility, analysis the cause why government should assume responsibility for primary healthcare system, discuss the specific content and form of government responsibility of Primary healthcare, it will provide a reference for the of state Legislature.
    The effect of TLR3 signaling pathway on tumer cell apoptosis
    Xiao-Jiao GAO Li CHEN,
    2014, 34(10):  1430-1433. 
    Asbtract ( 100 )   PDF (472KB) ( 522 )  
    Related Articles | Metrics
    TLR3,a pattern recognition receptor(PRR), recognizes pathogen associated molecular patterns (PAMPs) double-stranded RNA(dsRNA) to initiate immunity response. Recent publications demonstrated that TLR3 played an important role in promoting cells apoptosis in a range types of cells.Particularly, TLR3 tends to inducing cell apoptosis in tumor cells.This provides a potential evidence for tumor therapy by dsRNA.
    Research progress on immunomodulatory effects of ICOS/ICOSL and related diseases
    2014, 34(10):  1434-1437. 
    Asbtract ( 154 )   PDF (458KB) ( 487 )  
    Related Articles | Metrics
    Inducible co-stimulator(ICOS)and its ligand(ICOSL)play an important role in the response and regulation of immune system. It shows that ICOS bind to ICOSL relating to self-immune diseases and tumour. Targeted interventions of ICOS/ICOSL will provide new approaches for prevention and therapy of clinical diseases.
    Mechanism of neuropsychiatric disorders in Cushing’s syndrome
    Chen-Die YANG Bing XING
    2014, 34(10):  1438-1441. 
    Asbtract ( 159 )   PDF (553KB) ( 470 )  
    Related Articles | Metrics
    Cushing's syndrome describes the signs and symptoms associated with prolonged exposure to excess cortisol. Inappropriately high levels of the glucocorticoid harms the brain’s structure and function by damaging nerve cells, inducing apoptosis of neurons, suppressing neurogenesis, modulating synaptic plasticity, etc. Thus neuropsychiatric disorders as depression and cognitive impairment appear, with or without hippocampal atrophy. Surgery and medical treatment like mifepristone may improve those symptoms.
    Impact of cancer-associated fibroblasts derived from mesenchymal stem cell on tumor growth
    2014, 34(10):  1442-1445. 
    Asbtract ( 88 )   PDF (427KB) ( 13053 )  
    Related Articles | Metrics
    CAFs (carcinoma-associated fibroblasts) are a rate-limiting determinant for growth and metastasis of cancers in tumor microenvironment. Studies recently have shown that MSCs (mesenchymal stem cells) can mainly differentiate to CAFs by TGF-β/Samd signaling pathways, and contribute to tumor growth, invasion, angiogenesis , metastasis through direct cell contacts and paracrine of various kinds of cytokines.
    Human Chemokine receptor-like 1 and the relation with disease
    2014, 34(10):  1446-1449. 
    Asbtract ( 102 )   PDF (462KB) ( 622 )  
    Related Articles | Metrics
    Chemokine receptor-like 1 is sharing receptor of Chemerin and resolvin E1. After chemokine receptors 1 and its specific ligand had binded, intracellular calcium were stimulated to release, NF-κB、ERK1 and other signalings cascade activation reaction were leaded, it has been shown to be associated with inflammation, autoimmune disease, diabetes, metabolic diseases, cardiovascular diseases, bone diseases, tumors, reproductive system diseases, mental diseases and pathogenesis of liver diseases.
    Teaching Practice and Thinking Medical functional experiment
    2014, 34(10):  1450-1452. 
    Asbtract ( 91 )   PDF (431KB) ( 496 )  
    Related Articles | Metrics
    Objective To improve the effectiveness of medical functional experiment teaching. Methods The medical literature functional experiment teaching aspects of the collection and collation, and functional experiment teaching of medical problems in summarized, finally proposed solutions. Results Through the data collected for analysis, there exist Medical functional experiment teaching a lot of problems, which largely affected the results of medical functional experiment teaching, which requires about teaching workers must be further strengthened teaching Practice and medical functional thought experiment. Conclusion Medical functional experiment teaching theory and practice can be linked closer to the actual teaching methods can effectively guide students to actively yourself, learn and consolidate theoretical knowledge, has a very clear teaching effect from the experiment.