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ECV304 Cells (ecv304 + cell)

Distribution by Scientific Domains
Medical Sciences60%

Selected Abstracts

LC-MS analysis for the components captured by ECV304 cell from extract of Aconitum szechenyianum Gay.

BIOMEDICAL CHROMATOGRAPHY, Issue 4 2009
Jiang-Feng Yuan
Abstract A novel method of cell affinity screening (CAS), cell affinity capture coupled with LC-MS analysis, was developed for screening the bioactive compounds related to cardiovascular diseases from the natural product libraries. One of the major characteristics lies in its function in affinity-capturing and separating the bioactive components from the natural product libraries in vitro. Another characteristic is its use in analyzing and identifying the target compounds, by employing high-performance liquid chromatography and mass spectrometry. CAS was used for screening the bioactive components from the alkaloid extract derived from Aconitum szechenyianum Gay. Of the five components found to be bound to the oxidative-damaged endothelial cells, the two compounds identified, mesaconitine and aconitine, were recognized in the literature as being related to cardiovascular diseases. Copyright © 2008 John Wiley & Sons, Ltd. [source]

Comparison of anti-inflammatory activities of ruscogenin, a major steroidal sapogenin from Radix Ophiopogon japonicus, and Its succinylated derivative, RUS-2HS

DRUG DEVELOPMENT RESEARCH, Issue 4 2008
Ya-Lin Huang
Abstract Ruscogenin (RUS), first isolated from Ruscus aculeatus, is also a major steroidal sapogenin of the traditional Chinese herb Radix Ophiopogon japonicus. It has robust anti-inflammatory activities. In previous studies, a ruscogenin affinity column, derived from succinylated ruscogenin (RUS-2HS), was used to purify an antibody of ruscogenin. A ruscogenin affinity column can also be used to explore its protein targets. However, until now there have been no related pharmacological reports about ruscogenin derivatives. Whether the activity groups of ruscogenin have been blocked during the derivation process remains unknown. The present study was performed to compare the anti-inflammatory activities in vitro of RUS-2HS and ruscogenin. Both compounds reduced tumor necrosis factor-, (TNF-,)-induced adhesion of human pro-myelocytic leukemia cells (HL-60) to endothelial ECV304 cells with IC50 values of 6.90,nM and 7.45,nM, respectively. They were also inhibited overexpression of ICAM-1 in ECV304 cells at the mRNA level as evaluated by real-time PCR and at the protein level evaluated by flow cytometry with similar potency. Such data demonstrate that the functional groups of ruscogenin were not blocked by derivation, suggesting further use of the ruscogenin affinity column for target investigation. Meanwhile, RUS-2HS was found to have remarkable anti-inflammatory activity for the first time, indicating it would be a new lead compound with improved bioavailability. Drug Dev Res 69: 196,202, 2008. © 2008 Wiley-Liss, Inc. [source]

Paradoxical enhancement of oxidative cell injury by overexpression of heme oxygenase-1 in an anchorage-dependent cell ECV304

JOURNAL OF CELLULAR BIOCHEMISTRY, Issue 3 2004
Keiko Maruhashi
Abstract There has been increasing evidence suggesting the potent anti-inflammatory roles of heme oxygenase-1 (HO-1) in protecting renal tubular epithelial cells, vascular endothelial cells, and circulating monocytes. Based on these findings, novel therapeutic interventions have been proposed to control the expression of endothelial HO-1 levels to ameliorate various vascular diseases. We evaluated the effect of HO-1 gene transfer into an anchorage-dependent cell, ECV304. Effect of HO-1 production on the cell injury induced by hydrogen peroxide was evaluated after hemin stimulation and after HO-1 gene transfection. Morphological changes and the induction of various anti-apoptotic proteins were examined at the same time. Levels of HO-1 expression were variable in different clones of HO-1-transfected ECV304 cells. Among these, the clones with moderate levels of HO-1 expression were significantly more resistant to oxidative stress. In contrast, those with the highest levels of HO-1 exhibited paradoxically enhanced susceptibility to oxidative injury. Interestingly, the cell survival after oxidative stress was in parallel with the levels of Bcl-2 expression and of fibronectin receptor, ,5 integrin. It is suggested from these results, that excessive HO-1 not only leads to enhanced cell injury, but also prolongs the repair process of the injured endothelial tissue. However, HO-1 reduces the oxidative cell injury and protects the endothelial cells, if its expression is appropriately controlled. © 2004 Wiley-Liss, Inc. [source]

Bisphenol A diglycidyl ether (BADGE) is a PPAR, agonist in an ECV304 cell line

BRITISH JOURNAL OF PHARMACOLOGY, Issue 4 2000
David Bishop-Bailey
Peroxisome proliferator activated receptors (PPAR)s are nuclear transcription factors of the steroid receptor super-family. One member, PPAR,, a critical transcription factor in adipogenesis, is expressed in ECV304 cells, and when activated participates in the induction of cell death by apoptosis. Here we describe a clone of ECV304 cells, ECV-ACO.Luc, which stably expresses a reporter gene for PPAR activation. ECV-ACO.Luc respond to the PPAR, agonists, 15-deoxy-,12,14 PGJ2, and ciglitizone, by inducing luciferase expression. Furthermore, using ECV-ACO.Luc, we demonstrate that a newly described PPAR, antagonist, bisphenol A diglycidyl ether (BADGE) has agonist activities. Similar to 15-deoxy-,12,14 PGJ2, BADGE induces PPAR, activation, nuclear localization of the receptor, and induces cell death. British Journal of Pharmacology (2000) 131, 651,654; doi:10.1038/sj.bjp.0703628 [source]