Hydrogen sulfide attenuates hepatic ischemia-reperlusion injury: role of antioxidant and antiapoptotic signaling

Hydrogen sulfide (H...S) is an endogenously produced gaseous signaling molecule with diverse physiological activity. The potential protective effects of H...S have not been evaluated in the liver. The purpose of the current study was to investigate if H...S could afford hepatoprotection in a murine...

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Bibliographic Details
Published in:American journal of physiology. Heart and circulatory physiology 2008-08, Vol.295 (2), p.H801
Main Authors: Jha, Saurabh, Calvert, John W, Duranski, Mark R, Ramachandran, Arun, Lefer, David J
Format: Article
Language:English
Subjects:
Antioxidants
Hydrogen sulfide
Liver diseases
Molecules
Proteins
Studies
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Summary:Hydrogen sulfide (H...S) is an endogenously produced gaseous signaling molecule with diverse physiological activity. The potential protective effects of H...S have not been evaluated in the liver. The purpose of the current study was to investigate if H...S could afford hepatoprotection in a murine model of hepatic ischemia-reperfusion (I/R) injury. Hepatic injury was achieved by subjecting mice to 60 min of ischemia followed by 5 h of reperfusion. H...S donor (IK1001) or vehicle were administered 5 min before reperfusion. H2S attenuated the elevation in serum alanine aminotransferase (ALT) by 68.6% and aspartate aminotransferase (AST) by 70.8% compared with vehicle group. H...S-mediated cytoprotection was associated with an improved balance between reduced glutathione (GSH) vs. oxidized glutathione (GSSG), an attenuated formation of lipid hydroperoxides, and an increased expression of thioredoxin-1 (Trx-1). Furthermore, H...S inhibited the progression of apoptosis after I/R injury by increasing the protein expression of heat shock protein (HSP-90) and Bcl-2. These results indicate that H...S protects the murine liver against I/R injury through an upregulation of intracellular antioxidant and antiapoptotic signaling pathways. (ProQuest: ... denotes formulae/symbols omitted.)
ISSN:0363-6135
1522-1539