Search results for: Sodium nitroprusside CAS: [13755-38-9]
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Neurotoxic effects of interleukin-6 and sodium nitroprusside on cultured rat hippocampal neurons.
The neurotoxicity of interleukin-6 (IL-6) and sodium nitroprusside (SNP, CAS 13755-38-9) was examined using primary cultures of rat hippocampal neurons. The cell viability was significantly reduced after the cultures were co-incubated with IL-6 4, 40, 400 ng/ml or SNP 1, 10, 100 mumol/l for 24 h. In addition, N omega-nitro-L-arginine (NNA, CAS 2149-70-4) at 0.1 mmol/l, when co-added with IL-6 400 ng/ml in cultures, significantly increased IL-6 reduced viability from 78.3 +/- 6.7% to 113.3 +/- 10.0%. These results indicate that IL-6 exerts neurotoxicity on cultured hippocampal neurons probably via overformation of nitric oxide in cultures.T C Ma, X Z Zhu
2313 related Products with: Neurotoxic effects of interleukin-6 and sodium nitroprusside on cultured rat hippocampal neurons.
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Comparison of the effects of ularitide acetate and other bronchorelaxing substances on the thrombin-induced permeability raise of human endothelial cell monolayers.
Endothelial cell contraction plays a pivotal role in vascular leakage. It increases the extravasation of fluid and macromolecules from the lumen into the interstitium. This is also true for bronchial edema. Previous studies have indicated that an elevation of intracellular adenosine-3',5'-cyclic monophosphate (cAMP) or guanosine-3',5'-cyclic monophosphate (cGMP), respectively, can counteract this vascular leakage by improving the endothelial barrier function in analogy to the relaxation of smooth muscle cells. To investigate the potential antiedemateous effects of ularitide acetate (CAS 115966-23-9), isoproterenol hemisulfate (CAS 6078-56-4), sodium nitroprusside (CAS 13755-38-9, SNP), aminophylline (CAS 317-34-0), and combinations of these compounds, their effects on thrombin-induced macromolecular permeability raise in relation to cGMP- or cAMP-levels, respectively, in a model of human umbilical vein endothelial cells (HUVECs) were examined. Ularitide acetate, isoproterenol hemisulfate, and SNP all increased the amount of cyclic nucleotides and decreased the raise in permeability in the following order of potency: isoproterenol hemisulfate > ularitide acetate > SNP. Aminophylline raised both cGMP- and cAMP-levels in a weaker amount and was not able to decrease the thrombin-induced permeability raise on its own. By way of contrast, preincubation of HUVECs with aminophylline resulted in a more than additive potentiation of the cGMP-levels and the permeability lowering induced by ularitide-acetate. These in vitro-data indicate that ularitide-acetate, especially in combination with phosphodiesterase (PDE) inhibitors, could probably have beneficial effects in bronchial permeability edema.C Korn, R Neidlein, K Strein, O H Wilhelms