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1.
Article in Chinese | WPRIM | ID: wpr-910588

ABSTRACT

Objective:To determine the clinical efficacy of selective decongestive devascularization of gastrosplenic (SDD-GSR) and splenectomy combined with pericardial vascularization in the treatment of portal hypertension in cirrhosis.Methods:A total of 134 patients with cirrhosis portal hypertension admitted to the First Affiliated Hospital of Wenzhou Medical University were enrolled in the study, including 102 males and 32 females, with an average age of 51 years. Of 61 cases of SDD-GSR were included in the SDD-GSR group, and 73 cases of splenectomy combined with pericardial vascularization were included in the control group. Preoperative and postoperative white blood cell count, platelet count, Child-Pugh grade of liver function, free portal pressure (FPP) and postoperation tomplication were analyzed in the two groups. Operation time, intraoperative blood loss, free portal pressure (FPP), Child-Pugh grade of liver function, preoperative and postoperative white blood cell count, platelet count, and postoperative complications were analyzedin the two groups.Results:The operation time and intraoperative blood loss of SDD-GSR group were 165 (110, 198) min and 280 (100, 650) ml, which were lower than those of control group [190 (135, 605) min and 895 (300, 3 500) ml], the differences were statistically significant ( P<0.05). Postoperative FPP of SDD-GSR group and control group was 39 (35, 44) cmH 2O (1 cmH 2O=0.098 kPa) and 38 (34, 44) cmH 2O, respectively, which were lower than those before operation, with statistical significance (both P<0.05). Postoperative platelet count and white blood cell count in SDD-GSR group were lower than those in control group, and the differences were statistically significant (all P<0.05). The Child-Pugh grading of recent postoperative liver function in SDD-GSR group was better than that in control group, with statistical significance ( P<0.05). The complication rate (abdominal infection and portal vein thrombosis) of control group was higher than SDD-GSR group. Conclusion:SDD-GSR is better than splenectomy combined with pericardial vascularization since it has less intraoperative bleeding, obvious improvement of liver function and fewer complications, and it may be an effective surgical option for the treatment of portal hypertension of cirrhosis.

2.
Article in Chinese | WPRIM | ID: wpr-756271

ABSTRACT

Objective To evaluate safety and effectiveness of endoscopic retrograde cholangiopancreatography ( ERCP ) for patients with decompensated cirrhosis combined with choledocholithiasis. Methods A retrospective analysis was performed on data of 79 patients with decompensated cirrhosis combined with choledocholithiasis, 92 patients with chronic viral hepatitis, and 114 patients without liver disease who underwent ERCP at the First Hospital of Lanzhou University from December 2012 to December 2016. Intraoperative operating conditions, postoperative improvement of liver function indices, and complications among the three groups were compared and analyzed. Results The level of serum prothrombin time before ERCP in patients with cirrhosis (12. 9±2. 2) s was higher than that in patients with chronic viral hepatitis (12. 1±1. 9) s and those without liver disease (11. 7±1. 4) s, the difference was statistically significant ( F=21. 530, P<0. 001) . Operating time in patients with cirrhosis was longer than that of two other groups ( 58. 58 ± 19. 40 min VS 52. 53 ± 16. 74 min VS 49. 81 ± 14. 82 min, F=6. 444, P = 0. 002 ) . In patients with cirrhosis, postoperative liver function indices of aspartate aminotransferase ( 66. 0 IU/L VS 53. 0 IU/L) , alanine aminotransferase ( 61. 0 IU/L VS 52. 0 IU/L) ,γ-glutamyltransferase ( 318. 0 IU/L VS 231. 0 IU/L ) , alkaline phosphatase ( 232. 0 μmol/L VS 210. 0 μmol/L) , and total bilirubin ( 65. 7 μmol/L VS 56. 3 μmol/L ) were all lower compared with preoperative ones ( all P<0. 05) . No perforation or death occurred in the three groups. There were 3 cases ( 3. 8%) of mild bleeding at duodenal papilla after endoscopic sphincteropapillotomy in cirrhosis patients, i.e., 2 cases of Child-Pugh C and 1 case of Child-Pugh B. Errhysis occurred in one case ( 1. 27%) of Child-Pugh C patient at lower esophagus varices. There were no statistical differences on incidences of complications among the three groups ( P>0. 05) . Conclusion ERCP is safe and effective for Child-Pugh A and B patients with decompensated cirrhosis combined with choledocholithiasis. Liver function and blood coagulation function should be improved in Child-Pugh C patients before ERCP.

3.
Article in Chinese | WPRIM | ID: wpr-819074

ABSTRACT

Objective: To explore the effect of microRNA(miR)-222 on cell proliferation and apoptosis of fibroblasts in hypertrophic scar (HS) and the underlying mechanisms. Methods: The expression of miR-222 in the HS and the normal skin tissues was detected by real-time RT-PCR. The HS fibroblasts were transfected with miR-222 mimic and miR-222 inhibitor respectively. The cell viability was tested with MTT assay, cell cycle distribution and apoptosis were detected with flow cytometry and the expression levels of proliferation, apoptosis and cell cycle related proteins were determined with Western blot. Direct target of miR-222 was evaluated by dual-luciferase reporter assay. Results: miR-222 was significantly up-regulated in HS tissues compared with normal skin tissues(PConclusion: miR-222 enhances cell proliferation and inhibits cell apoptosis of HS fibroblasts through negative regulation of MMP1, which suggests that miR-222 and MMP1 might be used as novel biomarkers and targets in diagnostic and therapeutic approaches for HS.


Subject(s)
Apoptosis , Genetics , Cell Proliferation , Genetics , Cicatrix, Hypertrophic , Fibroblasts , Humans , Matrix Metalloproteinase 1 , Metabolism , MicroRNAs , Metabolism
4.
Journal of Clinical Pediatrics ; (12): 421-424, 2017.
Article in Chinese | WPRIM | ID: wpr-618976

ABSTRACT

Objective To explore the factors influencing serum trough concentration of vancomycin in pediatric patients with severe gram-positive cocci pneumonia. Methods The general information, the biochemical test results, and plasma concentration of vancomycin were collected from 93 pediatric patients with severe gram-positive cocci pneumonia. The relative factors influencing trough concentration of vancomycin were analyzed retrospectively. Results With the dosage of 40-60 mg/(kg·d), serum trough concentration of vancomycin were between 10-20 mg/L in 26 patients, <10 mg/L in 54 cases, ≥20 mg/L in 13 cases. The ALT, AST, GFR, and γ-GT were significantly different among three groups (P<0.05); the 10-20 mg/L group had the highest levels of AST and γ-GT, the ≥20 mg/L group had the highest level of ALT and the lowest level of GFR. Multiple linear regression analysis showed that GFR was negatively linearly correlated with the serum trough concentration of vancomycin (R2=0.039, P<0.05). The median serum trough concentration of vancomycin in pediatric patients with GFR≥90, 60–90, 30–60 mL/(min·1.73m2) were 8.66, 18.21, 8.45 mg/L respectively, and the difference is statistically significant (P<0.05). Conclusions The serum trough concentration of vancomycin is negatively linearly correlated with GFR in pediatric patients with severe gram-positive cocci pneumonia. The patients with impaired renal function are easier to reach the target serum trough concentration of vancomycin. Clinical use of vancomycin should follow the low doses in the range the guideline recommended, and the serum trough concentration should be closely monitored.

5.
Article in Chinese | WPRIM | ID: wpr-468839

ABSTRACT

Objective To evaluate a new method for the isolation of rat pancreatic stellate cells (PSCs) and to investigate the influence of adipose derived stem cells (ADSCs) on PSCs in vitro.Methods Normal rat PSCs was isolated by collagenase and Optiprep density gradient centrifugation.The coculture system of ADSCs and PSCs was set up by transwell insert.The proliferation of PSCs was tested by CCK-8 test kit.Smoothmuscle α-actin (α-SMA) expression of PSCs were tested by Western blot.The apoptosis of HSCs was tested by flow cytometer.The cytokines in the culture solution were tested by ELISA kit.Results The quantity of PSCs was above 5 × 106 cells per rat.The purity and the viability of the cells were about 90-97 percent.After coculture for 72 h,the proliferation and activation of PSCs was inhibited by ADSCs (F =223.27,P < 0.05 ; F =52.97,P < 0.05) and the apoptosis of PSCs was promoted by ADSCs (F =43.62,P < 0.05).more NGF and less TGF-β1 was secreted by ADSCs than by PSCs (NGF:14.68 ± 0.94 vs.8.31 ±0.86,t =4.67,P <0.05;TGF-β1:10.65 ±0.46 vs.70.47 ±0.99,t =21.72,P<0.01).Conclusions ADSCs inhibit the proliferation and activation of PSCs by ADSCs secreting cytokines.

6.
Chinese Journal of Digestion ; (12): 742-747, 2014.
Article in Chinese | WPRIM | ID: wpr-469268

ABSTRACT

Objective To compare the difference between bone marrow stomal cell (BMSC) and adipose-derived stem cell (ADSC) of liver fibrosis in rats.Methods BMSC and ADSC of Sprague-Dawley (SD) rats were isolated and purified.The stem cell markers were detected with flow cytometry.The coculture system was set up with 0.4 μm Transwell insert semipermeable membrane.ADSC or BMSC were co-cultured with hepatic stellate cells (HSC).Normal hepatocyte cell line of rat (BRL) was co-cultured with HSC as negative control group and HSC cultured alone was blank control group.After cultured for 72 hours,the proliferation of HSC was determined by cell counting kit-8 (CCK-8) method.The expression of α-smooth muscle actin (α-SMA) of HSC was detected by Western blotting.The apoptosis of HSC was examined by flow cytometry.After BMSC,ADSC and BRL cultured alone for 72 hours,expression level vascular endothelial growth factor (VEGF),interleukin-10 (IL-10),nerve growth factor (NGF) and transforming growth factor-β1 (TGF-β1) in the culture medium were detected by enzymelinked immunosorbent assay (ELISA) method.The rats model of liver fibrosis were established.The rats were divided into BMSC treatment group,ADSC treatment group,BRL group and culture medium group,six rats in each group,which were injected with 1.5 mL BMSC,ADSC and BRL cells suspension (5 × 106) through portal vein,respectively,and same volume of culture medium was injected to the rate of culture medium group,once every two weeks for four weeks.The pathological changes of liver tissue sections were observed and liver fibrosis markers were tested.T test was performed for comparison between two samples and analysis of variance was used for comparison among multiple groups.Results BMSC and ADSC were successfully isolated and cultured.The phenotype of BMSC and ADSC was similar.Compared with blank control group and negative control group,both ADSC and BMSC could inhibit the proliferation of HSC and promote apoptosis (proliferation,2.43±0.27,2.39±0.33,1.92±0.38 and 2.18±0.31,FBMSC =25.61,FADSC =38.63,both P<0.05 ;apoptosis rate,(5.59 ± 0.40)%,(6.82±0.57)%,(8.31± 1.03) % and (9.36 ± 0.54) %,FBMSC =73.69,FADSC =97.41,both P< 0.05).The effects of ADSC were more significant than those of BMSC (t=5.76 and 5.18,both P<0.05).There was difference in the cytokine levels secreted by ADSC and BMSC (NGF,(7.46 ± 0.54) pg/mL vs (3.95 ± 0.71) pg/mL,t =10.92,P<0.05; TGF-β1,(8.79 ±0.93) pg/mL vs (6.36±0.85) pg/mL,t=7.58,P<0.05).The cell transplantation experiment indicated that both BMSC and ADSC had significant inhibitory effect on liver fibrosis.The activity index of inflammation and degree of fibrosis in BMSC treatment group and ADSCs treatment group were 9.87±2.07,4.17 ± 0.94 and 10.13 ± 1.81,3.98 ± 0.82,which were significantly lower than those in blank control group (13.78±2.53 and 5.09±1.15)and negative control group (13.34± 1.89 and 4.95± 1.22,FBMSC=51.26 and 32.29,P<0.05; FADSC =46.73 and 40.94,P<0.05).The level of hyaluronic acid ((191.5±33.2) μg/L and (178.8±28.2) μg/L),type Ⅲ collagen ((19.9±5.1) μg/L and (21.7± 3.3) μg/L) and hydroxyproline ((312.6±38.8) μg/g and (325.8±28.2) μg/g) of BMSC treatment group and ADSC treatment group were significantly lower than those of negative control group and blank control group (hyaluronic acid,(282.3 ± 18.7) μg/L and (287.5 ± 26.7) μg/L),F =73.51 ; type Ⅲ collagen,(35.3± 3.3) μg/L and (32.5±4.3) μg/L,F=76.19; hydroxyproline,(458.4 ± 38.1) μg/g and (473.9 ± 63.7) μg/g,F=60.37,all P<0.05).However,there was no difference between BMSC treatment group and ADSC treatment (all P<0.05).Conclusions ADSC and BMSC had similar stem cell characteristics.There was difference in inhibiting the activation of HSC between ADSC and BMSC.But there was no significant difference in inhibiting liver fibrosis of rats in vivo.

7.
Article in Chinese | WPRIM | ID: wpr-443417

ABSTRACT

Objective To investigate the effect of capsaicin on hepatic stellate cells (HSCs) and liver fibrogenesis.Methods HSCs were cultured.The reactive oxygen in HSCs under capsaicin at different concentrations was tested by DCFH-DA kit.The proliferation of HSCs was detected by CCK-8 test kit.Smoothmuscle α-actin (α-SMA) expression of HSCs was evaluated by Western blot.The fibrosisrelated genes were tested by RT-PCR.The apoptosis of HSCs was measured by flow cytometer.Bcl-2,bax and cyt-c was detected by Western blot.A murine model of liver fibrogenes was established.Capsaicin of different concentration was injected intraperitoneally.Liver pathology was observed using HE staining.Hydroxyproline content of liver and levels of collagen Ⅲ and hyaluronic acid in serum were tested.Results In dose dependent manner capsaicin inhibited the generation of the reactive oxygen species.Proliferation and activation of HSCs was inhibited by capsaicin (respectively F =13.267,57.392,all P < 0.05) and the apoptosis of HSCs was promoted by capsaicin (F =235.571,P < 0.05).Bax,cyt-c and caspase-3 was increased obviously (respectively F =29.334,38.274,138.329,all P < 0.05).Capsaicin changed the expression of fibrosis-related genes (TGF-β1,TIMP-1) in HSCs (respectively F =376.534,253.751,all P <0.05).Capsaicin downregulated the level of hydroxyproline,collagen Ⅲ and hyaluronic acid in the rat model (respectively F =153.397,27.149,38.392,all P < 0.05).Conclusions Capsaicin inhibits the proliferation and activation of hepatic stellate cells.Capsaicin promotes the apoptosis of hepatic stellate cells,and inhibits liver fibrogenesis.

8.
Journal of Chinese Physician ; (12): 1627-1629,1633, 2014.
Article in Chinese | WPRIM | ID: wpr-601231

ABSTRACT

Objective To investigate the effect of hepatic stellate cells (HSC) on proliferation and invasion of hepatocellular carcinoma cells and the possible mechanism involved.Methods The HSC was isolated by optiprep method.Methyl thiazolyl tetrazolium(MTT) assay was used to detect the proliferation of hepatocellular carcinoma cells.The effect of invasion was measured with transwell assay.Matrix metalloproteinase-2 (MMP-2) and nuclear factor-κB (NF-κB) were detected by Western blotting.Results HSC was isolated and cultured successfully.HSC promoted the proliferation and invasion of hepatocellular carcinoma cells (proliferation:0.571 ±0.024 vs 0.803 ±0.048,1.271 ±0.044,1.973 ±0.036; invasion:25.2 ± 1.9 vs 35.8 ±3.3,44.4 ±2.7,53.9 ±3.6) (P <0.05).MMP-2 (1.32 ±0.22 vs 2.46 ±0.39) and NF-κB(0.85 ±0.09 vs 1.44 ±0.21) were increased obviously in hepatocellular carcinoma cells stimulated by HSC.Conclusions HSC can promote the proliferation and invasion of hepatocellular carcinoma cells.The mechanism might be related to up-regulation of the expressions of MMP-2 and NF-κB.

9.
Article in Chinese | WPRIM | ID: wpr-435036

ABSTRACT

Objective To study the protective effects of resveratrol against hepatic stellate cells (HSCs) and liver fibrogensis.Methods HSCs were isolated from liver of SD rats.The reactive oxygen output in HSCs under resveratrol in different concentrations was tested by DCFH-DA kit.The proliferation of HSCs was tested by CCK-8 test kit.Smoothmuscle α-actin (α-SMA) expression of HSCs was evaluated by Western blotting.The activity-related genes were measured by PCR.The models of liver fibrogenes were established.Resveratrol in different concentrations was administrated intraperitoneally.Liver was studied by pathology and SMA staining.Hydroxyproline content of liver and levels of collagen Ⅲ and hyaluronic acid in serum were tested.Results HSCs were isolated from liver and cultured successfully.Resveratrol inhibited the generation of the reactive oxygen.Proliferation and activation of HSCs was inhibited by resveratrol (0.536 ±0.052,0.411 ±0.047,0.327 ±0.063,0.312 ±0.032,F =12.776,P <0.05) (103 ±7,90 ±7,63 ± 4,53 ± 3,F =62.179,P < 0.05).Resveratrol inhibited the expression of genes (myogenic determination gene MyoD,collagen 11 and collagen Ⅰ) in HSCs(122 ± 5,96 ± 3,68 ± 3,60 ± 3,F =180.600,P<0.05) (100±8,82 ±3,53 ±3,51 ±2,F=77.451,P <0.05) (170 ±3,147 ±4,92 ±3,90 ±2,F =462.878,P < 0.05).Resveratrol downregulated the level of hydroxyproline,collagen Ⅲ and hyaluronic acid (358.3 ± 20.2,320.5 ± 15.3,290.3 ± 24.5,F =23.929,P < 0.05) (32.8 ± 3.1,28.9 ±1.3,25.3±1.8,F=20.050,P<0.05)(276.3 ±17.8,225.3 ±28.3,195.4 ±11.2,F=18.585,P<0.05).Conclusions Resveratrol can inhibit the proliferation and activation of HSCs and downregulate the fibrogensis level of the liver of rats.

10.
Article in Chinese | WPRIM | ID: wpr-442709

ABSTRACT

Objective To investigate the Fsp27 gene's influence on the regulation of hepatic stellate cells (HSCs) in vitro.Methods HSCs were isolated from rat liver,the Fsp27 gene was detected in primary HSCs,and activated HSCs were detected by RT-qPCR.After 72 h of Fsp27 transduction through a lentivirus expressing Fsp27 (pLV-Fsp27),the proliferation of HSCs was tested by the CCK-8 test kit,smooth muscle α-actin (α-SMA) expression of HSCs was tested by Western blot,and the fibrosis-related genes were tested by RT-qPCR.Results The HSCs were isolated and cultured successfully,and the Fsp27 genetic difference between primary and activated HSCs was significant (P<0.01).After coculture for 72 h,Fsp27 inhibited the proliferation and activation of HSCs (P<0.05).Fsp27 can enhance expression of the MMP-2 gene and down-regulate expression of the TIMP-1 and TGF-β1 gene in activated HSCs (P<0.05).Conclusion The Fsp27 gene can inhibit the proliferation and activation of HSCs,regulate the expression of fibrosis-related genes,and may play an important role in maintaining the quiescent phenotype of HSCs.

11.
Article in Chinese | WPRIM | ID: wpr-442133

ABSTRACT

Objective To explore the effects of adipose tissue-derived stem cells (ADSCs) on the proliferation and invasion of pancreatic cancer cell lines in vitro.Methods ADSCs were isolated and co-cultured with pancreatic cancer cells.The proliferation and invasion of pancreatic cancer cells was tested by CCK-8 test kit.Stromal cell derived factor (SDF-1),vascular endothelial growth factor(VEGF),matrix metalloproteinase(MMP-9)and transforming growth factor-β (TGF-β1)in the culture medium were assayed by ELISA.The expression of cytokines in pancreatic cancer cells and ADSCs were detected by qRT-PCR.CCK-8 test kit was used to measure the AMD3100 regulation for the co-culture of ADSCs and pancreatic cancer cells.Results ADSCs can promote the proliferation and invasion of pancreatic cancer cells (all P <0.05); more SDF-1,VEGF,MMP-9 and less TGF-β1 was secreted by ADSCs than by pancreatic cancer cells(SDF-1:1100±100 vs.0 vs.0,F=389.134,P<0.01;VEGF:140±4 vs.99±5 vs.93 ±4,F=174.102,P <0.05;MMP-9:61.8 ±4.2 vs.43.5 ±2.8 vs.54.5 ±3.0,F=76.279,P<0.05;TGF-β1:20.6 ±3.0 vs.35.6 ±2.6 vs.41.3 ±5.5,F =79.338,P <0.05).ADSCs promote the expression of VEGF and MMP-9 in pancreatic cancer cells(VEGF:63.7 ±5.9 vs.50.6 ±4.1,t =7.536,P<0.05; MMP-9:mRNA(55.8±3.6 vs.42.7 ±3.1,t =8.279,P<0.05).AMD3100 significantly downregulates these growth-promoting effects of ADSCs on pancreatic cancer cells(SW1990:1.539 ±0.140 vs.1.361±0.066,t=2.835,P<0.05;PANC-1:1.376±0.100 vs.1.281±0.031,t=2.860,P<0.05).Conclusions ADSCs promote the proliferation and invasion of pancreatic cancer cells.

12.
Journal of Chinese Physician ; (12): 1028-1031, 2013.
Article in Chinese | WPRIM | ID: wpr-441778

ABSTRACT

Objective To investigate the influence of fat-specific protein 27 (Fsp27) gene on the regulation of liver fibrogenesis in vivo.Methods Hepatic stellate cells (HSCs) were isolated from rat liver.Fsp27 gene was detected in primary HSCs and activated HSCs by real-time quantitative PCR (RTqPCR).Lentiviral vector carrying Fsp27 gene was constructed.The model of liver fibrosis was established by infusing carbon tetrachloride (CC14).The rats with liver fibrogenesis were infected by the virus.Liver sections were made to observe the structure and form of liver histocytes.The content of fibrous protein in liver and serum was detected by enzyme-linked immunosorbent assay (ELISA) and radioimmunoassay.Resukts HSCs were isolated and cultured successfully.The difference of Fsp27 gene between primary HSCs and activated HSCs was significant(P < 0.01).The model of liver fibrosis was achieved.After infecting the model rats,we found the fibrosis level in treatment group was lower compared with control group.Conclusions Fsp27 treatment can decrease collagen deposition in the liver and inhibit the formation of fibrosis.

13.
Article in Chinese | WPRIM | ID: wpr-419418

ABSTRACT

Objective To investigate the influence of low bilirubin level on hepatic stellate cells (HSCs) in vitro. Methods HSCs were isolated and cultured from the liver of SD rats. The effect of bilirubin in different concentration on reactive oxygen in HSCs was determined by DCFH-DA kit. The proliferation of HSCs was tested by CCK-8 test kit.Smoothmuscle α-actin (α-SMA) expression of HSCs was tested by Western blot.The apoptosis of HSCs was tested by flow cytometry.The fibrosis-related genes were tested by PCR. Results HSCs were isolated and cultured successfully.Bilirubin in low concentration (0,1,10,20 mg/L) inhibited the generation of the reactive oxygen.Proliferation and α-SMA expression of HSCs was inhibited by bilirubin (0.624 ± 0.092,0.536 ± 0.127,0.407 ± 0.033,0.399 ± 0.022,F =13.454,P <0.05 ; 339 ± 2,336 ± 10,246 ± 7,242 ± 5,3.7 ± 0.3,F =191.107,P < 0.05 ) and the apoptosis of HSCs was promoted by bilirubin(2.69 ±0.07%,2.95 ±0.10%,4.41 ±0.22%,4.91 ±0.86%,F =34.731,P <0.05 ).Bilirubin in low concentration changed the expression of fibrosis-related genes in HSCs.The ratio of TIMP-1mRNA/MMP-2mRNA decreased (54 ± 2,65 ± 2,47 ± 2,44 ± 2,F =73.400,P < 0.05).Conclusions Bilirubin in low concentration inhibits the proliferation and activation of hepatic stellate cells,orobablv bv a mechanism in which bilirubin promoted antioxidative function.

14.
Article in Chinese | WPRIM | ID: wpr-424391

ABSTRACT

Objective To establish human pancreatic cancer xenografts in nude mice, and to investigate the antitumor efficacy of human endostatin expressed by replication-competent adenovirus AdTPHre-hE in vivo. Methods Pancreatic cancer cells AsPC-1 were injected subcutaneously in BALB/c nude mice to establish the xenografts. Tumor growth was observed and measured after AdTPHre-hE treatment. Expression of endostatin was detected by ELISA assay. The tumors were harvested for pathologic examination and immunohistochemical staining. Results Tumors grew more slowly in the AdTPHre-hE group and their sizes were markedly smaller than those of the Ad-hE group (P<0.01)and control group(P<0. 01). Endostatin levels were detected in the sera of nude mice in all treated groups, and endostatin expression in AdTPHre-hE group increased with time. The endostatin level in the AdTPHre-hE treated group was much higher(P<0. 01)and increased faster than that in the Ad-hE treated group. Immunohistochemical staining for Hexon of adenovirus capsid showed more positive tumor cells in the tumor tissues treated with AdTPHre-hE. Immunohistochemical staining for FⅧ revealed a decreased microvessel density in the tumor tissues treated with AdTPHre-hE. Conclusion The replication-competent adenovirus efficiently expressed high-level endostatin and significantly inhibited tumor growth in vivo.

15.
Chinese Journal of General Surgery ; (12): 1027-1030, 2011.
Article in Chinese | WPRIM | ID: wpr-423413

ABSTRACT

Objective To investigate the effect of adipose derived stem cells (ADSCs) on hepatic stellate cells (HSCs) in vitro and on liver fibrosis in vivo.Methods ADSCs and HSCs were isolated from adipose tissue and liver respectively in SD rats.The coculture system was set up by transwell insert.The 5th passage HSCs were cultured on the 6-well plastic plate,and ADSCs or BRLs seeded on the transwell insert.The proliferation of HSCs was tested by CCK-8 test kit.Smoothmuscle α-actin (α-SMA) expression of HSCs were tested by Western blot.Rat models of liver fibrosis was established.Rats in ADSCs treatment group were infused with ADSCs and those in control group were infused with Buffalo rat liver cells (BRLs).Liver sections were studied by immunocytochemistry.Liver hydroxyproline (Hyp) content,serum laminin (LN)and hyaluronic acid (HA) were tested,the cytokines in the culture medium were assayed.Results HSCs and ADSCs were isolated successfully.After coculture for 72 h,compared with the control group,the proliferation and activation of HSCs was inhibited by ADSCs( absorbance of each group were 2.172 ±0.107,1.424 ± 0.013,1.209 ± 0.117,F =90.605,P < 0.05 ; Gray-scale values of each group were 1.4 ± 0.2,152 ± 14,258 ± 18,F =283.348,P < 0.05 ),ADSCs infusion inhibits liver fibrosis in model rats ( F =77.234,65.164,58.309,all P < 0.05 ).More hepatocyte growth factor(HGF) and less transforming growth factor-β1 (TGF-β1) (F=1.767,P<0.05)and nerve growth factor (NGF) (F=2.301,P<0.05) were secreted by ADSCs than by BRLs.Conclusions ADSCs inhibit the proliferation and activation of hepatic stellate cells.Treatment with ADSCs decreases collagen deposition in the liver and inhibits liver fibrosis.

16.
Article in Chinese | WPRIM | ID: wpr-417027

ABSTRACT

Objective To evaluate perfusion computed tomography in the assessment of portal vein pressure changes in an experimental dog model of liver cirrhosis and portal hypertension.Methods The canine model of cirrhosis and portal hypertension was induced by portal vein stenosis with combination of systemic thioacetamide(TAA) feeding in drinking water.All of the Beagles in control group and cirrhotic group underwent hepatic perfusion on a spiral CT scanner.The parameters of hepatic perfusion were calculated by the method of deconvolution.The portal vein pressure was measured by a laparotomy surgery.Results ① In control group, the portal vein pressure was ( 14.5 ± 2.2) cm H2O, while it was (23.1 ± 2.8) cm H2O in PHT group, there was significant difference in the portal vein pressure between the two groups (P<0.05).② The blood flow(BF) was (112 ±14) ml·100 g-1·min-1 in controls, while ( 96 ± 11) ml·100 g-1·min-1 in PHT group; the blood volume ( BV ) in control group and PHT group was (10 ±3) ml·100 g-1 and (11 ± 5) ml· 100 g-1, respectively; the mean transit time( MTT) was (7.1 ± 2.0) s and (10.4 ± 3.5) s, respectively; the hepatic arterial fraction (HAF) was ( 24 ± 5) % and ( 37 ± 6)% , respectively; the hepatic arterial perfusion (HAP) was(27 ±6) ml·100 g-1·min-1 and (35 ±5) ml·100 g-1·min-1, respectively; the portal venous perfusion (PVP) was (85 ± 13) ml·100 g-1·min-1 and (61 ±11) ml·100 g-1·min-1, respectively.There was significant difference in all parameters between the two groups except the parameter BV(P < 0.05).③ In PHT group, the PVP and BF were negatively correlated with the portal vein pressure, while positively correlated with MTT and HAF.Portal vein pressure was negatively correlated with PVP, the equation, Y = 36.624 -0.219X, was deduced with linear regression analysis, by which the portal vein pressure in PHT Beagles was ( 23.2 ± 2.4) cm H2O, which was correlated with the observed by laparotomy value (23.1 ± 2.8) cm H2O (r = 0.843, P < 0.05).Conclusion CT perfusion is a new non-invasive and effective method for assessment of portal vein pressure.

17.
Article in Chinese | WPRIM | ID: wpr-416642

ABSTRACT

Objective To develop a double-regulated replicative adenovirus carrying the Human endostatin gene(hEndo). Methods The plasmid pTPHre-hEndo was constructed by gene engineering technique, carrying human endostatin gene, in which El A gene and E1B gene were driven by human telomerase reverse transcriptase (hTERT) promoter and hypoxia response element (HRE) promoter,respectively. The pTPHre-hEndo was co-transfected with pBHGE3 in 293 cells to generate recombinant adenovirus AdTPHre-hEndo. Virus titer was measured by the TCID50 method. Virus replication assay was performed to evaluate the selective replication ability of AdTPHre-hEndo. The transgene expression of endostatin was detected by ELISA assay. Results A novel gene-viral therapeutic system AdTPHre-hEndo was constructed by gene engineering technique and its titer was 3. 25 X 1010 pfu/ml.Proliferative test revealed that AdTPHre-hEndo could proliferate selectively in telomerase positive tumors. Furthermore, in comparison with non-replicative adenovirus Ad-hEndo, the transgene expression of endostatin mediated with AdTPHre-hEndo was significantly increased (P < 0. 01).Conclusion The novel gene-viral therapeutic system AdTPHre-hEndo has the capacity to replicate in pancreatic cancer cells and expresses the endostatin efficiently, and may provide a new strategy for pancreatic cancer gene therapy.

18.
Article in Chinese | WPRIM | ID: wpr-384834

ABSTRACT

Objective To explore the ideal choice of feeding artery which is used for regional arterial infusion (RAI) in severe acute pancreatitis. Methods Forty-five patients with SAP were treated with RAI. The ideal feeding artery was that can supply entire pancreas according to arteriography and can maximize concentration of drug at pancreatic tissue. The pancreatic arteriography was considered as the final objective evidence for choice. Results (1)Gastroduodenal artery was chosen as feeding artery in forty-four cases, and superior mesenterlc artery was chosen in only one case because of vascular abnormity. (2)According to splenic arteriography, blood of splenic artery was supplied to spleen chiefly, and only partial tail of pancreas was applied by splenic artery. (3)According to celiac trunk arteriography, blood of celiac trunk could be supplied to entire pancreas, but a considerable proportion of the total blood was supplied to spleen through splenic artery and liver through hepatic artery proper.Therefore, the drug utilization index was lower. (4)According to gastroduodenal arteriography, blood of gastroduodenal artery could be supplied to entire pancrea, and almost all of the blood that contains drug flowed into pancreas. Therefore, the drug utilization index was higher. Conclusions Gastroduodenal artery is the ideal choice of artery which is used for regional intra-arterial infusion in sever acute pancreatitis. Pancreatic arteriography should be applied routinely when yever acute pancreatitis was treated with RAI.

19.
Article in Chinese | WPRIM | ID: wpr-391315

ABSTRACT

Objective To evaluate the curative effect of selective decongestive devascularization shunt of gastrosplenic region(SDDS-GSR) for the treatment of portal hypertension. Methods From September 2000 to June 2008, 44 patients with portal hypertension had received SDDS-GSR in our hospital. Twenty-nine of them had been followed up for 12-85 months (mean=44months). Results Operative mortality was 0 %. Mesenteric area pressure(33.82±5.12 cm H_2O) was higher than splenic area pressure(24.57±4.63 cm H_2O)soon after the operation finished(P<0.01). No re-bleeding ca-ses were found, and the encephalopathy occurred in 2.27% of the patients in the early stage of post-operation. However, the rates of 3.45% for re-bleeding and 3.45% for encephalopathy were noticed in long-term follow-up. The 1-, 3- and 5-year survival were 100%, 95% and 95%, respectively. Dur-ing the long-term follow-up, the platelet counts markedly increased from (49.2±21.8 × 10~9/L) of preoperative value to (77.2±29.5×10~9/L) (P<0.01), while spleen size was significantly reduced.Conclusion SDDS-GSR is a reliable and reasonable surgical procedure for the management of portal hypertension.

20.
Article in Chinese | WPRIM | ID: wpr-390432

ABSTRACT

Objective To construct the adenovirus vector containing mice CD40- IgG2aFc-IRS-GFP fusion gene and detect the expression of the fusion protein in transfeete 293cells.Methods The fragments of CD40, IgG2aFc were obtained and inserted into plasmid PDC316-IgG2aFc-GFP.After being verified by sequencing, Ad5-PDC316-CD40-IgG2aFc-GFP was contransfored with the bckbone vector into 293 cells.The virus titer was detected after replicating and purifing and the expression of the fusion protein was analyzed.Results A virus and plasmid were constructed successfully.The vitro infection showed that the virus can infect cells of which the fusion protein was confirmed by fluo-rescence.The expression of the fusion protein increased with the increased time and virus concentra-tion.The protein expression stopped increasing after the virus concentration came to a certain level.Conclusion CD40, IgG2aFc fragments are correctly ligated with plasmid PDC316-IgG2aFc-GFP, and the fusion protein can be expressed in 293cells.This might lay a foundation for further studies of the expresstion of virus, immune tolerance and mechanism of liver transplantation model in rats.

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