摘要
Background Glioma-induced edema is considered as one of the most pathological characteristics of glioma and a significant source of morbidity and mortality. New strategies are needed for the treatment of peritumoral edema in glioma. Endostatin has been proven to be beneficial as an anti-angiogenic agent in experimental gliomas, but the effects are unclear. This study aimed to investigate the effects of endostatin on C6 glioma-induced edema. Methods Tumorigenic mice were established by subcutaneous injection of three glioma cell lines, C6-null cells and stable transfected-C6 cells overexpressing mock vector （C6-mock cells） and endostatin （C6-endo cells）. Endostatin expression in xenograft C6 glioma was determined by immunostaining and Western blotting. Glioma-induced edema and tumor vessel permeability were assayed. The effect of endostatin on vascular enodothelial growth factor （VEGF） expression in vivo was analyzed by quantitative polymerase chain reaction （Q-PCR） and enzyme-linked immunosorbent assay （ELISA）. The number of vesiculo-vascuolar organelles （VVOs） formed in tumor endothelia was calculated using electron microscopy. Data were analyzed by using one-way analysis of variance （ANOVA） followed by Dunnett＇s post hoc test for multiple comparisons to the control groups. Results Overexpression of endostatin （C6-endo cells） significantly suppressed tumor growth and reduced tumor edema and vessel permeability. ELISA analysis showed that the level of VEGF protein was markedly decreased in tumor from C6-endo cells compared with tumor from C6-null cells and C6-mock cells. Similar results were obtained by Q-PCR. Furthermore, the number of VVOs observed in tumor from C6-endo mice was significantly reduced compared with tumor from C6-null cells or C6-mock cells. Conclusions Our data provide primary evidence that endostatin reduces glioma-induced edema and vascular permeability. Using endostatin may be an effective strategy for treating glioma edema.
Background Glioma-induced edema is considered as one of the most pathological characteristics of glioma and a significant source of morbidity and mortality. New strategies are needed for the treatment of peritumoral edema in glioma. Endostatin has been proven to be beneficial as an anti-angiogenic agent in experimental gliomas, but the effects are unclear. This study aimed to investigate the effects of endostatin on C6 glioma-induced edema. Methods Tumorigenic mice were established by subcutaneous injection of three glioma cell lines, C6-null cells and stable transfected-C6 cells overexpressing mock vector （C6-mock cells） and endostatin （C6-endo cells）. Endostatin expression in xenograft C6 glioma was determined by immunostaining and Western blotting. Glioma-induced edema and tumor vessel permeability were assayed. The effect of endostatin on vascular enodothelial growth factor （VEGF） expression in vivo was analyzed by quantitative polymerase chain reaction （Q-PCR） and enzyme-linked immunosorbent assay （ELISA）. The number of vesiculo-vascuolar organelles （VVOs） formed in tumor endothelia was calculated using electron microscopy. Data were analyzed by using one-way analysis of variance （ANOVA） followed by Dunnett＇s post hoc test for multiple comparisons to the control groups. Results Overexpression of endostatin （C6-endo cells） significantly suppressed tumor growth and reduced tumor edema and vessel permeability. ELISA analysis showed that the level of VEGF protein was markedly decreased in tumor from C6-endo cells compared with tumor from C6-null cells and C6-mock cells. Similar results were obtained by Q-PCR. Furthermore, the number of VVOs observed in tumor from C6-endo mice was significantly reduced compared with tumor from C6-null cells or C6-mock cells. Conclusions Our data provide primary evidence that endostatin reduces glioma-induced edema and vascular permeability. Using endostatin may be an effective strategy for treating glioma edema.
