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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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