Journal
AMINO ACIDS
Volume 41, Issue 1, Pages 205-215Publisher
SPRINGER WIEN
DOI: 10.1007/s00726-011-0834-1
Keywords
S-Propargyl-cysteine; Nuclear factor-kappa B; Inflammatory response; Hydrogen sulfide; Reactive oxygen species
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Funding
- National Basic Research Program of China (973 Program) [2010CB912600]
- National Science Fund for Distinguished Young Scholars [30888002]
- Synthetic Department of Research and Development Technique of New Drugs [2009ZX09301-011]
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The present study attempts to investigate the effects of S-propargyl-cysteine (SPRC), a sulfur-containing amino acid, on lipopolysaccharide (LPS)-induced inflammatory response in H9c2 cardiac myocytes. We found that SPRC prevented nuclear factor-kappa B (NF-kappa B) activation assessed by NF-kappa B p65 phosphorylation and I kappa B alpha degradation, suppressed LPS-induced extracellular signal-regulated kinase 1/2 (ERK1/2) phosphorylation and intracellular reactive oxygen species (ROS) production. Furthermore, incubation of H9c2 cells with SPRC induced phosphorylation of Akt in a time- and concentration-dependent manner. In addition, SPRC attenuated LPS-induced mRNA and protein expression of tumor necrosis factor-alpha (TNF-alpha), and mRNA expression of intercellular adhesion molecule-1 (ICAM-1) and inducible nitric oxide synthase (iNOS). The effects of SPRC were abolished by cystathionine gamma-lyase [CSE-an enzyme that synthesizes hydrogen sulfide (H2S)] inhibitor, dl-propargylglycine (PAG), SPRC-induced Akt phosphorylation and TNF-alpha release was also abolished by the phosphoinositide 3-kinase (PI3K) inhibitor LY294002. Furthermore, SPRC also increased LPS-induced down-regulation expression of CSE and H2S level in H9c2 cells. PAG abolished SPRC-induced up-regulation of H2S level. Therefore, we concluded that SPRC produced an anti-inflammatory effect in LPS-stimulated H9c2 cells partly through the CSE/H2S pathway by impairing I kappa B alpha/NF-kappa B signaling and by activating PI3K/Akt signaling pathway.
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