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This Article Full Text Full Text (PDF) All Versions of this Article: 295/2/H801    most recent 00377.2008v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Google Scholar Articles by Jha, S. Articles by Lefer, D. J. PubMed PubMed Citation Articles by Jha, S. Articles by Lefer, D. J.

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

¹Department of Medicine, Division of Cardiology, Albert Einstein College of Medicine, Bronx, New York; and ²Department of Surgery, Division of Cardiothoracic Surgery, Emory University School of Medicine, Atlanta, Georgia

Submitted 10 April 2008 ; accepted in final form 12 June 2008

Hydrogen sulfide (H₂S) is an endogenously produced gaseous signaling molecule with diverse physiological activity. The potential protective effects of H₂S have not been evaluated in the liver. The purpose of the current study was to investigate if H₂S 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. H₂S 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. H₂S-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, H₂S 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 H₂S protects the murine liver against I/R injury through an upregulation of intracellular antioxidant and antiapoptotic signaling pathways.

apoptosis; liver; glutathione; thioredoxin; heat shock protein 90

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