Hydrogen sulfide (H 2 S) is increasingly recognized as an important signaling molecule in the cardiovascular and nervous systems. Recently, H 2 S donors were reported to induce neutrophil apoptosis and to suppress expression of some leukocyte and endothelial adhesion molecules. Using rats, we examined the possibility that H 2 S is an endogenous regulator of key inflammatory events at the leukocyte-endothelial interface. Via intravital microscopy, we observed that H 2 S donors (NaHS and Na 2 S) inhibited aspirin-induced leukocyte adherence in mesenteric venules (ED 50 of 5.0 µmol/kg for Na 2 S), likely via activation of ATP-sensitive K + (K ATP ) channels. Inhibition of endogenous H 2 S synthesis elicited leukocyte adherence. Leukocyte infiltration in an air pouch model was also suppressed by H 2 S donors (NaHS, Lawesson’s reagent, and N-acetylcysteine; ED 50 of 42.7, 1.3, and 29.9 µmol/kg, respectively) and exacerbated by inhibition of endogenous H 2 S synthesis. Carrageenan-induced paw edema was suppressed by H 2 S donors (NaHS and Na 2 S; ED 50 s of 35 and 28 µmol/kg, respectively) to the same extent as by diclofenac and enhanced by an inhibitor of H 2 S synthesis. Suppression of edema formation by H 2 S donors was mimicked by a K ATP channel agonist and reversed by an antagonist of this channel. These results suggest that endogenous H 2 S is an important mediator of acute inflammation, acting at the leukocyte-endothelium interface. These findings have important implications for anti-inflammatory drug development.—Zanardo, R. C. O., Brancaleone, V., Distrutti, E., Fiorucci, S., Cirino, G., Wallace, J. L. Hydrogen sulfide is an endogenous modulator of leukocyte-mediated inflammation.
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Hydrogen sulfide is an endogenous modulator of leukocyte-mediated inflammation
Zanardo, Renata C. O.; Brancaleone, Vincenzo; Distrutti, Eleonora; Fiorucci, Stefano; Cirino, Giuseppe; Wallace, John L.
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, Volume 20 (12): 2118
Fed of American Socs for Experimental Biology – Oct 1, 2006
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