paba/infarction

Acute myocardial infarction (AMI) is associated with vascular inflammation, including activation and adherence of neutrophils to vascular endothelial cells via CD11b/CD18 intercellular adhesion molecule interactions. Myeloperoxidase (MPO) induces CD11b surface expression in polymorphonuclear

Therapy for stroke is undergoing major changes. Many of the changes parallel the advances made in the therapy for myocardial infarction. Acute intervention with cytoprotective and thrombolytic agents is undergoing active investigation. Cytoprotective therapy includes drugs that act to prevent cell

OBJECTIVE Inhibitors of poly (ADP-ribose) synthetase (PARS) activity reduce the infarct size caused by regional myocardial ischaemia and reperfusion in the rabbit and rat in vivo. The mechanism of action of these inhibitors is unclear. Here we investigate the effects of the PARS inhibitor

Various triacsin C analogs, containing different alkenyl chains and carboxylic acid bioisoteres including 4-aminobenzoic acid, isothiazolidine dioxide, hydroxylamine, hydroxytriazene, and oxadiazolidine dione, were synthesized and their inhibitions of long chain fatty acyl-CoA synthetase (ACSL) were

The effect of the Poly (adenosine 5'-diphosphate ribose) synthetase (PARS) inhibitor 3-aminobenzamide on (i) infarct size caused by regional myocardial ischaemia (60 min) and reperfusion (3 h) in the anaesthetised pig, and (ii) on the cell injury/necrosis of human cardiomyoblasts caused by hydrogen

Myeloperoxidase (MPO) is a pro-inflammatory enzyme abundantly secreted by activated myeloid cells after stroke. We show that when MPO activity is either blocked by the specific inhibitor 4-aminobenzoic acid hydrazide (ABAH) in wildtype (WT) mice or congenitally absent (MPO-/-), there was decreased

Few effective treatment options exist for stroke beyond the hyperacute period. Radical generation and myeloperoxidase (MPO) have been implicated in stroke. We investigated whether pharmacologic reduction or gene deletion of this highly oxidative enzyme reduces infarct propagation and improves