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ANTECEDENT HYDROGEN SULFIDE ELICITS AN ANTI‐INFLAMMATORY PHENOTYPE IN POSTISCHEMIC MURINE SMALL INTESTINE: ROLE OF HEME OXYGENASE‐1
Author(s) -
Yusof Mozow,
Peyton Kelly,
Kalogeris Theodore,
Gaskin F. Spencer,
Fay William,
Durante William,
Korthuis Ronald J.
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.1138.8
Subject(s) - heme oxygenase , chemistry , heme , hydrogen sulfide , pharmacology , microcirculation , ischemia , biochemistry , medicine , enzyme , sulfur , organic chemistry
We recently demonstrated that preconditioning with an exogenous hydrogen sulfide donor (H 2 S) donor (NaHS‐PC) 24 h prior to ischemia and reperfusion (I/R) causes postcapillary venules to shift to an anti‐inflammatory phenotype in C57Bl/6 WT mice such that these vessels fail to support increased postischemic leukocyte rolling (LR) and adhesion (LA). The objective of the present study was to determine whether heme oxygenase‐1 (HO‐1) is an effector of the anti‐inflammatory effects noted during I/R in mice preconditioned with NaHS. I/R induced marked increase in LR and LA, effects that were prevented by NaHS‐PC. Treatment with the HO inhibitor SnPPIX, but not the inactive protoporphyrin CuPPIX, just prior to I/R prevented the anti‐inflammatory effects of antecedent NaHS. We then evaluated the effect of NaHS as a preconditioning stimulus in mice that were genetically deficient in HO‐1 (HO‐1 −/− in the H129 background with appropriate WT controls). NaHS‐PC was ineffective in HO‐1−/− mice. Our data provides a novel effector mechanism by which H 2 S preconditioning is protective in the microcirculation. Supported by AA14945 and DK43785.