Objective: To investigate the effects of static magnetic field(SMF) on the viability, adhesion molecule expression of human umbilical vessel endothelial cell. Methods: Magnetic flux intensity was 0. 1 mT, 1 mT, 10 mT....Objective: To investigate the effects of static magnetic field(SMF) on the viability, adhesion molecule expression of human umbilical vessel endothelial cell. Methods: Magnetic flux intensity was 0. 1 mT, 1 mT, 10 mT. Cell viability and proliferation were measured with 3H-TdR and MTT methods; and apoptosis of human umbilical vein endothelial cell (HUVEC) was studied by flow cytometry and transmission electric microscopy. ELISA was used to measure the expression of ICAM-1 and VCAM-1 on endothelium. Results: 0. 1 mT SMF had no effects on the growth of HUVEC. however,SMF of 1 mT, 10 mT attenuated growth of HUVEC. 10 mT static magnetic field could induce apoptosis and necrosis of HUVEC. 10 mT SMF enhanced the expression of ICAM-1 and VCAM-1 on endothelium. Conclusion: The effect of SMF depends on the intensity of SMF. 10 mT SMF has adverse effects on human umbilical vessel endothelial cell.展开更多
Objective To examine the inhibitory effects of recombinant purified arresten on tumor formation. Methods Purified arresten protein was incubated with human umbilical vein endothelial cells (HUVECs) and HeLa cells in v...Objective To examine the inhibitory effects of recombinant purified arresten on tumor formation. Methods Purified arresten protein was incubated with human umbilical vein endothelial cells (HUVECs) and HeLa cells in vitro. The effect on proliferation of HUVECs and HeLa cells was examined using 3-(4,5)-dimethylthiahiazo (-z-y1)-3,5-di-phenytetrazoliumromide assay, and apoptosis of these cells monitored by flow cytometry. The effect on migration of HUVECs and HeLa cells was examined by Boyden chamber. Twenty colon carcinoma-bearing C67BL/6 mice were used to investigate the antitumor effects of arresten protein. The mice were randomly divided into arresten treatment group (n=10) and control group (n=10). The microvessel densities of the tumors were measured by immunohistochemical staining with anti-CD31 monoclonal antibody. Results Arresten inhibited the proliferation and migration of HUVECs in a dose-dependent manner while promoting apoptosis. However, arresten had no significant effects on the proliferation and apoptosis of HeLa cells. The migration of HeLa cells was modestly inhibited by arresten. The arresten treatment group of mice showed no weight loss or unusual behavior during the course of treatment, and the tumor growth was significantly decreased; in contrast, the control group of mice exhibited rapidly growing tumors and cachexia. A dramatically decreased microvessel density in tumor tissues was found in arresten-treated mice compared with that in the control mice. Conclusion Arresten can inhibit tumor growth through inhibition of tumor angiogenesis.展开更多
Objective To investigate the potential effects of angiogenic process by secretory phospholipase A2 (sPLA2)inhibitor-HyPE(linking N-derivatized phosphatidyl-ethanolamine to hyaluronic acid)on human bone marrow endothel...Objective To investigate the potential effects of angiogenic process by secretory phospholipase A2 (sPLA2)inhibitor-HyPE(linking N-derivatized phosphatidyl-ethanolamine to hyaluronic acid)on human bone marrow endothelial cell line(HBME-1). Methods In order to examine the suppressing effects of HyPE on HBME-1 proliferation, migration, and capillary-like tube formation, HBME-1 were activated by angiogenic factor, specifically by basic fibroblast growth factor(b-FGF), vascular endothelial growth factor(VEGF),and oncostatin M(OSM)(at a final concentration of 25, 20, and 2.5 ng/mL, respectively), then HBME-1 proliferation, migration, and tube forma-tion were studied in the absence or presence of HyPE. HBME-1 tube formation was specially analyzed in fibrin gel. Results HyPE effectively inhibited HBME-1 proliferation and migration as a dose-dependent manner, whatever HBME-1 were grown in the control culture medium or stimulated with b-FGF, VEGF, or OSM. In fibrin, the formations of HBME-1 derived tube-like structures were enhanced by all angiogenic factors, but these were strongly suppressed by HyPE. Conclusions The results support the involvement of sPLA2 in angiogenesis. It is proposed that sPLA2 inhibitor introduces a novel approach in the control of cancer development.展开更多
文摘Objective: To investigate the effects of static magnetic field(SMF) on the viability, adhesion molecule expression of human umbilical vessel endothelial cell. Methods: Magnetic flux intensity was 0. 1 mT, 1 mT, 10 mT. Cell viability and proliferation were measured with 3H-TdR and MTT methods; and apoptosis of human umbilical vein endothelial cell (HUVEC) was studied by flow cytometry and transmission electric microscopy. ELISA was used to measure the expression of ICAM-1 and VCAM-1 on endothelium. Results: 0. 1 mT SMF had no effects on the growth of HUVEC. however,SMF of 1 mT, 10 mT attenuated growth of HUVEC. 10 mT static magnetic field could induce apoptosis and necrosis of HUVEC. 10 mT SMF enhanced the expression of ICAM-1 and VCAM-1 on endothelium. Conclusion: The effect of SMF depends on the intensity of SMF. 10 mT SMF has adverse effects on human umbilical vessel endothelial cell.
基金Supported by Key Scientific and Technological Project of Shanxi Province (042082)Technological and Engineering Project of the Department of Education of Shanxi Province (20080017)
文摘Objective To examine the inhibitory effects of recombinant purified arresten on tumor formation. Methods Purified arresten protein was incubated with human umbilical vein endothelial cells (HUVECs) and HeLa cells in vitro. The effect on proliferation of HUVECs and HeLa cells was examined using 3-(4,5)-dimethylthiahiazo (-z-y1)-3,5-di-phenytetrazoliumromide assay, and apoptosis of these cells monitored by flow cytometry. The effect on migration of HUVECs and HeLa cells was examined by Boyden chamber. Twenty colon carcinoma-bearing C67BL/6 mice were used to investigate the antitumor effects of arresten protein. The mice were randomly divided into arresten treatment group (n=10) and control group (n=10). The microvessel densities of the tumors were measured by immunohistochemical staining with anti-CD31 monoclonal antibody. Results Arresten inhibited the proliferation and migration of HUVECs in a dose-dependent manner while promoting apoptosis. However, arresten had no significant effects on the proliferation and apoptosis of HeLa cells. The migration of HeLa cells was modestly inhibited by arresten. The arresten treatment group of mice showed no weight loss or unusual behavior during the course of treatment, and the tumor growth was significantly decreased; in contrast, the control group of mice exhibited rapidly growing tumors and cachexia. A dramatically decreased microvessel density in tumor tissues was found in arresten-treated mice compared with that in the control mice. Conclusion Arresten can inhibit tumor growth through inhibition of tumor angiogenesis.
文摘Objective To investigate the potential effects of angiogenic process by secretory phospholipase A2 (sPLA2)inhibitor-HyPE(linking N-derivatized phosphatidyl-ethanolamine to hyaluronic acid)on human bone marrow endothelial cell line(HBME-1). Methods In order to examine the suppressing effects of HyPE on HBME-1 proliferation, migration, and capillary-like tube formation, HBME-1 were activated by angiogenic factor, specifically by basic fibroblast growth factor(b-FGF), vascular endothelial growth factor(VEGF),and oncostatin M(OSM)(at a final concentration of 25, 20, and 2.5 ng/mL, respectively), then HBME-1 proliferation, migration, and tube forma-tion were studied in the absence or presence of HyPE. HBME-1 tube formation was specially analyzed in fibrin gel. Results HyPE effectively inhibited HBME-1 proliferation and migration as a dose-dependent manner, whatever HBME-1 were grown in the control culture medium or stimulated with b-FGF, VEGF, or OSM. In fibrin, the formations of HBME-1 derived tube-like structures were enhanced by all angiogenic factors, but these were strongly suppressed by HyPE. Conclusions The results support the involvement of sPLA2 in angiogenesis. It is proposed that sPLA2 inhibitor introduces a novel approach in the control of cancer development.
