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find Author "ZHAO Yunfeng" 3 results
  • Effects of lipopolysaccharide-binding protein inhibitory peptide on the binding of lipopolysaccharide to alveolar macrophages in a mouse model of endotoxemia

    Objective To investigate whether P12,a kind of lipopolysaccharide(LPS)-binding protein(LBP) inhibitory peptide,could suppress the binding of LPS to alveolar macrophages(AMs) in a mouse model of endotoxemia in vivo.Methods Forty mice were randomly divided into five groups,ie.a control group,an endotoxemia group,a low dose P12-treated group,a middle dose P12-treated group and a high dose P12-treated group.Mouse model of endotoxemia was established by LPS injection intraperitoneally in the endotoxemia group and P12-treated groups.P12 was instilled via the tail vein.The effects of P12 on the binding of LPS to AMs were determined by flow cytometric analysis and quantization by mean fluorescence intensity(MFI).The productions of tumor necrosis factor α(TNF-α) in serum of mice were measured by enzyme-linked immunosorbent assay(ELISA).Results MFI in AMs from low,middle and high dose P12-treated groups was 40.08%,30.76% and 24.45%,respectively,which was higher than that of the control group(4.61%),but less than that of the endotoxemic mice(45.31%).The concentration of TNF-α in serum of low,media and high dose P12-treated mice was (112.69±19.78)pg/mL,(86.34±9.25) pg/mL,(70.48±8.48)pg/mL respectively,which was higher than that of the control group[(24.88±5.82)pg/mL],but less than that of the endotoxemic mice[(180.17±39.14)pg/mL].Conclusion The results suggest that P12 inhibit the binding of LPS and AMs,thus reduce the proudction of TNF-α stimulated by LPS.

    Release date:2016-09-14 11:56 Export PDF Favorites Scan
  • Establishment of Budd-Chiari Syndrome Model in Rat

    Objective To explore the feasibility of the Budd-Chiari syndrome model establishment in rat by using the inferior vena cava coarctation. Methods Fifty SD rats were randomly divided into experimental group and sham operation group, the laparotomy was performed after general anesthesia by intraperitoneal injection, and dissociated the inferior vena cava. In the experimental group, the vena cava was tightly ligated with silk thread according to partial portal vein coarctation, enclosing 23 G L-style blunt needle in the ligature to prevent complete obliteration. The diameter of the vena cava was set to about 80% of its normal size after removing the 23 G L-style blunt needle. The abdominal Doppler, liver function, blood routine examination, and liver biopsy were tested at different time (on week 1, 4, 8, and 12) after operation. Results The signs of inferior vena cava and primary hepatic venous obstruction, liver congestion and cirrhosis, ascites, hepatosplenomegaly, portal vein extension, and collateral patency occurred on week 4 in the experimental group. The levels of AST, ALT, AKP, TBIL, DBIL, and TBA in the experimental group were significantly higher than those in the sham operation group (P<0.05), and the WBC, PLT, RBC, HGB, and ALB in the experimental group was significantly lower than those in the sham operation group (P<0.05). Conclusion The inferior vena cava coarctation can be successfully used to establish a rat model of Budd-Chiari syndrome.

    Release date:2016-09-08 10:34 Export PDF Favorites Scan
  • Immunoliposomes Containing Vasohibin Inhibit Pulmonary Fibrosis in Mice

    Objective To investigate the effects of immunoliposomes containing vasohibin on pulmonary fibrosis in mice. Methods Liposomes containing vasohibin plasmids were prepared by reverse phase evaporation technique, then combined with VWF antibody to form the immunoliposomes. 30 mice were randomly divided into a control group, a model group, and a vasohibin group. The mice in the model group and the vasohibin group were nasally instilled with bleomysin to induce pulmonary fibrosis. After 3 days, the mice in the vasohibin group were nasally instilled with the immunoliposomes containing vasohibin. The mice were all sacrificed after 14 days. Lung tissue sections were stained by HE and CD31 immunohistochemistry staining. The level of hydroxyproline in lung was measured by colorimetry. Results The resultsdemonstrated that the vasohibin immunoliposome could markedly decrease angiogenesis with the number of ( 46 ±16) compared to ( 78 ±12 ) , and decrease fibroblast proliferation with ( 0. 84 ±0. 12) μg/mg compared to ( 1. 39 ±0. 23) μg/mg. Conclusion The vasohibin immunoliposome can attenuate pulmonaryfibrosis and provide a novel strategy for clinical application in the future.

    Release date:2016-08-30 11:53 Export PDF Favorites Scan
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