Please use this identifier to cite or link to this item: https://doi.org/10.1089/ars.2009.2899
DC FieldValue
dc.titleThe effect of hydrogen sulfide donors on lipopolysaccharide-induced formation of inflammatory mediators in macrophages
dc.contributor.authorWhiteman, M.
dc.contributor.authorLi, L.
dc.contributor.authorRose, P.
dc.contributor.authorTan, C.-H.
dc.contributor.authorParkinson, D.B.
dc.contributor.authorMoore, P.K.
dc.date.accessioned2014-10-16T08:45:17Z
dc.date.available2014-10-16T08:45:17Z
dc.date.issued2010-05-15
dc.identifier.citationWhiteman, M., Li, L., Rose, P., Tan, C.-H., Parkinson, D.B., Moore, P.K. (2010-05-15). The effect of hydrogen sulfide donors on lipopolysaccharide-induced formation of inflammatory mediators in macrophages. Antioxidants and Redox Signaling 12 (10) : 1147-1154. ScholarBank@NUS Repository. https://doi.org/10.1089/ars.2009.2899
dc.identifier.issn15230864
dc.identifier.urihttp://scholarbank.nus.edu.sg/handle/10635/95225
dc.description.abstractThe role of hydrogen sulfide (H2S) in inflammation is controversial, with both pro- and antiinflammatory effects documented. Many studies have used simple sulfide salts as the source of H2S, which give a rapid bolus of H2S in aqueous solutions and thus do not accurately reflect the enzymatic generation of H2S. We therefore compared the effects of sodium hydrosulfide and a novel slow-releasing H 2S donor (GYY4137) on the release of pro- and antiinflammatory mediators in lipopolysaccharide (LPS)-treated murine RAW264.7 macrophages. For the first time, we show that GYY4137 significantly and concentration-dependently inhibits LPS-induced release of proinflammatory mediators such as IL-1β, IL-6, TNF-α, nitric oxide (•NO), and PGE2 but increased the synthesis of the antiinflammatory chemokine IL-10 through NF-κB/ATF-2/HSP-27-dependent pathways. In contrast, NaHS elicited a biphasic effect on proinflammatory mediators and, at high concentrations, increased the synthesis of IL-1β, IL-6, NO, PGE2 and TNF-α. This study clearly shows that the effects of H2S on the inflammatory process are complex and dependent not only on H2S concentration but also on the rate of H2S generation. This study may also explain some of the apparent discrepancies in the literature regarding the pro- versus antiinflammatory role of H2S. Antioxid. Redox Signal. 12, 1147-1154. © Copyright 2010, Mary Ann Liebert, Inc.
dc.description.urihttp://libproxy1.nus.edu.sg/login?url=http://dx.doi.org/10.1089/ars.2009.2899
dc.sourceScopus
dc.typeArticle
dc.contributor.departmentCHEMISTRY
dc.description.doi10.1089/ars.2009.2899
dc.description.sourcetitleAntioxidants and Redox Signaling
dc.description.volume12
dc.description.issue10
dc.description.page1147-1154
dc.description.codenARSIF
dc.identifier.isiut000276539300001
Appears in Collections:Staff Publications

Show simple item record
Files in This Item:
There are no files associated with this item.

SCOPUSTM   
Citations

228
checked on Apr 9, 2021

WEB OF SCIENCETM
Citations

219
checked on Apr 9, 2021

Page view(s)

69
checked on Mar 28, 2021

Google ScholarTM

Check

Altmetric


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.