cardiovascular-agents and sodium-bisulfide

Hydrogen sulfide (H(2)S) is a gasomediator synthesized from L- and D-cysteine in various tissues. It is involved in a number of physiological and pathological processes. H(2)S exhibits antiatherosclerotic, vasodilator, and proangiogenic properties, and protects the kidney and heart from damage following ischemia/reperfusion injury. H(2)S donors may be natural or synthetic, and may be used for the safe treatment of a wide range of diseases. This review article summarizes the current state of knowledge of the therapeutic function of H(2)S.

Topics: Angiogenesis Inducing Agents; Cardiovascular Agents; Cysteine; Diclofenac; Disulfides; Heart; Humans; Hydrogen Sulfide; Kidney; Levodopa; Prostaglandins F, Synthetic; Reperfusion Injury; Sulfides; Thioctic Acid; Thiones; Vasodilator Agents

We explored the effect of hydrogen sulfide (H(2)S) on atherosclerotic progression, particularly on intracellular adhesion molecule-1 (ICAM-1) in apolipoprotein-E knockout (apoE(-/-)) mice and human umbilical vein endothelial cells (HUVECs).. ApoE(-/-) mice were treated with sodium hydrosulfide (NaHS) or DL-propargylglycine (PPG); HUVECs were pretreated with NaHS. Compared with control mice, apoE(-/-) mice showed decreased plasma H(2)S level and aortic H(2)S production but increased plasma ICAM-1 and aortic ICAM-1 protein and mRNA. Compared with apoE(-/-) mice, apoE(-/-)+NaHS mice showed increased plasma H(2)S level, but decreased size of atherosclerotic plaque and plasma and aortic ICAM-1 levels, whereas apoE(-/-)+PPG mice showed decreased plasma H(2)S level but enlarged plaque size and increased plasma and aortic ICAM-1 levels. NaHS suppressed ICAM-1 expression in tumor necrosis factor (TNF)-alpha-treated HUVECs. NaHS inhibited IkappaB degradation and NF-kappaB nuclear translocation in HUVECs treated with TNF-alpha.. The vascular CSE/H(2)S pathway was disturbed in apoE(-/-) mice. H(2)S exerted an antiatherogenic effect and inhibited ICAM-1 expression in apoE(-/-) mice. H(2)S inhibited ICAM-1 expression in TNF-alpha-induced HUVECs via the NF-kappaB pathway.

Topics: Active Transport, Cell Nucleus; Alkynes; Animals; Aorta; Apolipoproteins E; Atherosclerosis; Body Weight; Cardiovascular Agents; Cells, Cultured; Cystathionine gamma-Lyase; Disease Models, Animal; Dose-Response Relationship, Drug; Endothelial Cells; Enzyme Inhibitors; Foam Cells; Glycine; Humans; Hydrogen Sulfide; I-kappa B Proteins; Intercellular Adhesion Molecule-1; Lipids; Male; Mice; Mice, Inbred C57BL; Mice, Knockout; Muscle, Smooth, Vascular; NF-kappa B; RNA, Messenger; Sulfides; Tumor Necrosis Factor-alpha

Topics: Animals; Aorta; Atherosclerosis; Cardiovascular Agents; Cystathionine gamma-Lyase; Endothelial Cells; Humans; Hydrogen Sulfide; Intercellular Adhesion Molecule-1; Muscle, Smooth, Vascular; Sulfides