Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P39060 (endostatin)
 2,284 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In order to establish the methods of high-performance liquid chromatography (HPLC) for determining the purity of recombinant human endostatin (rhEndostatin) and in vitro or in vivo activity of rhEndostatin, two columns were firstly used in HPLC analysis for determining the purity of rhEndostatin, including Waters Symmetry 300C4 (4.6 mm x 250 mm, 5 microm) and the Superdex75 HR 10/30. Cell lines, bovine capillary endothelial cells (BCEs) or human umbilical vein endothelial cells (HUVECs) expression human vascular endothelial growth factor (hVEGF) were used in method MTT or LDH as substrate, respectively. The bioactivity in vivo was assayed by the anti-tumor proliferation rate in H22 liver tumor-bearing mice. The results showed that the retention time of rhEndostatin sample was stable at 19.066 min or 11.506 min in reverse phase HPLC (RP-HPLC) or gel filtering HPLC (GF-HPLC). The stableness, repeat and recovery rates were over 99% in both methods and there was no statistical difference between these two methods (p > 0.05). In nonserum culture medium, rhEndostatin can sensitively and stably inhibit the proliferation of the HUVEC cells that were transfected with plasmid encoding hVEGF. LDH substrate methods is the most sensitive and stable method. The anti-tumor activity in H22 tumor-bearing mice was also highly repeatable and had an inhibition rate over 50% at 20 mg kg(-1) weight. As a conclusion, the RP-HPLC and GF-HPLC set up in this paper are highly repeatable, accurate and sensitive for detecting the purity of rhEndostatin. The bioactivity of rhEndostatin can be measured through detection the proliferation-inhibition on HUVECs transfectants with hVEGF in vitro or on H22 liver tumor in vivo.
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PMID:The methods for determining the purity and in vitro or in vivo activity of recombinant human endostatin. 1575 63

The angiogenesis system has been implicated in inflammatory and neoplastic processes; nevertheless, it has been little studied in relation to the pleural space. Our aim is to analyze pleural and plasma levels of the activators--vascular endothelial growth factor, basic fibroblastic growth factor, and inhibitors--endostatin and thrombospondin-1 and to estimate the association between these factors and related biochemical markers. We analyzed pleural fluid from 105 patients with one of the following types of pleural effusion: empyema or complicated parapneumonic, non-complicated parapneumonic, tuberculous, neoplastic and transudative. Angiogenesis activators were higher in exudates than in transudates (p < 0.001) and in empyema than in non-complicated parapneumonic patients (p < 0.001). Endostatin showed no significant differences. Trombospondin-1 showed higher levels in exudates than in transudates and in empyema than in non-complicated parapneumonic effusions (p < 0.001). In pleural exudates there was a positive correlation of angiogenesis activators and trombospondin-1 with low glucose and pH and high LDH. There was no correlation between pleural and plasma levels of the angiogenesis factors. We conclude that exudative pleural effusions showed higher vascular endothelial growth factor, basic-fibroblastic growth factor and trombospondin-1 values than transudative effusions that associated to low glucose and pH, and high LDH. There was no correlation between pleural and plasma concentrations, suggesting a compartmentalized response.
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PMID:Angiogenic factors and angiogenesis inhibitors in exudative pleural effusions. 1607 40