noc-18 has been researched along with Arteriosclerosis* in 2 studies
2 other study(ies) available for noc-18 and Arteriosclerosis
| Article | Year |
|---|---|
Urea induces macrophage proliferation by inhibition of inducible nitric oxide synthesis.
Atherosclerosis is a major cause of morbidity and mortality in chronic renal failure and is associated with the proliferation of macrophages within atherosclerotic lesions.. Because the progression of atherosclerosis as a consequence of decreased nitric oxide synthesis has been described, we investigated the correlation between the inhibition of inducible nitric oxide synthase (iNOS) by urea, macrophage proliferation as assayed by cell counting, tritiated thymidine incorporation and measurement of cell protein, and macrophage apoptosis.. Urea induces a dose-dependent inhibition of inducible nitric oxide synthesis in lipopolysaccharide-stimulated mouse macrophages (RAW 264.7) with concomitant macrophage proliferation. Macrophage proliferation, as determined by cell counting, became statistically significant at 60 mM urea, corresponding to a blood urea nitrogen level of 180 mg/100 ml, concentrations seen in uremic patients. iNOS protein expression showed a dose-dependent reduction, as revealed by immunoblotting when cells were incubated with increasing amounts of urea. The decrease of cytosolic DNA fragments in stimulated macrophages incubated with urea shows that the proliferative actions of urea are associated with a decrease of NO-induced apoptosis.. Our data demonstrate that the inhibition of iNOS-dependent NO production caused by urea enhances macrophage proliferation as a consequence of diminished NO-mediated apoptosis. Topics: Animals; Apoptosis; Arteriosclerosis; Benzoates; Cell Division; Cell Line; Diuretics, Osmotic; DNA Fragmentation; Enzyme Inhibitors; Hemoglobins; Imidazoles; Lipopolysaccharides; Macrophages; Mice; NG-Nitroarginine Methyl Ester; Nitric Oxide; Nitric Oxide Donors; Nitric Oxide Synthase; Nitric Oxide Synthase Type II; Nitroso Compounds; Urea | 1999 |
The formation of some antigenic epitopes in oxidized human low-density lipoprotein is inhibited by nitric oxide.
NO and NO-donors are able to inhibit the peroxidation of polyunsaturated fatty acids in human low-density lipoproteins (LDL) exposed to Cu+2. Here we report that 1-hydroxy-2-oxo-3,3-bis(3-aminoethyl)-1-triazene (NOC-18), a compound which releases NO at low rate in aqueous solutions, powerfully inhibits the peroxidation of polyunsaturated fatty acids, tryptophan loss, the formation of fluorescent aldehydic adducts in apo B100 and the increase of electrophoretic mobility in isolated LDL undergoing oxidation. The inhibitory effect is not restricted to Cu+2-induced peroxidation but is also detectable with other oxidizing conditions such as the free radical generator 2,2'-azobis-(2-amidino propane) hydrochloride (AAPH), the combination of horseradish peroxidase and H2O2 (HRP), and peroxynitrite (ONOO-). The recognition of Cu+2-, AAPH-, and ONOO(-)-modified LDL by specific autoantibodies present in serum of atherosclerotic patients is almost completely inhibited when the oxidation procedure is performed in the presence of NOC-18. However, NOC-18 is completely ineffective in preventing the formation of recognizable antigens in HRP-modified LDL. These findings suggest that NO may efficiently prevent the formation of some, but not all, the antigenic epitopes recognized by human autoantibodies and thus likely formed during in vivo LDL oxidation. Topics: Arteriosclerosis; Autoantibodies; Autoantigens; Copper; Epitopes; Humans; In Vitro Techniques; Lipid Peroxidation; Lipoproteins, LDL; Nitric Oxide; Nitroso Compounds; Oxidation-Reduction | 1997 |