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Am J Physiol Heart Circ Physiol (June 20, 2008). doi:10.1152/ajpheart.00377.2008
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Submitted on April 10, 2008
Revised on May 26, 2008
Accepted on June 12, 2008

Hydrogen Sulfide Attenuates Hepatic Ischemia-Reperfusion Injury: Role of Antioxidant and Anti-Apoptotic Signaling

Saurabh Jha1, John W. Calvert1, Mark R. Duranski1, Arun Ramachandran1, and David Joseph Lefer1*

1 Albert Einstein College of Medicine

* To whom correspondence should be addressed. E-mail: dlefer{at}aecom.yu.edu.

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. Therefore, the purpose of the current study was to investigate if H2S could afford hepatoprotection in a murine model of hepatic ischemia and reperfusion (I/R) Injury. Hepatic injury was achieved by subjecting mice to 60 min of ischemia followed by 5 hr of reperfusion. H2S donor (IK1001) or vehicle were administered 5 minutes before reperfusion. H2S attenuated the elevation in serum alanine aminotransferase (ALT) by 68.6% and aspartate aminotransferase (AST) by 70.8% compared to vehicle group. H2S-mediated cytoprotection was associated with an improved balance between reduced glutathione (GSH) vs. oxidized glutathione (GSSG),attenuated the formation of lipid hydroperoxides and increased expression of thioredoxin 1 (Trx-1). Furthermore H2S inhibited the progression of apoptosis following 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 anti-apoptotic signaling pathways. Key Words: hydrogen sulfide, antioxidant, apoptosis, ischemia-reperfusion.




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