Review Article

Role of Hydrogen Sulfide in Ischemia-Reperfusion Injury

Table 4

Effects of H2S and its donors in hepatic I/R injury.

Experimental modelsEffectsProposed mechanismsReferences

Hepatic I/R in vivo (rat)NaHS (28 μM/kg, prior to R) attenuates the injured hepatic function and the synthetic action of hepatocytesInhibition of lipid peroxidation and inflammation reactions[177]

Hepatic I/R in vivo (mice)NaHS (1.5 mg/kg, 1 h prior to I) protects against hepatic I/R injuriesActivation of the PtdIns3K-AKT1 pathway[17]

Hepatic I/R in vivo (rat)NaHS (14 μM/kg, 30 min prior to I) significantly attenuates the severity of liver injury and inhibits the production of lipid peroxidationAntioxidant and antiapoptotic activities[46]

Hepatic I/R in vivo (rat)DAS (1.75 mM/kg, 12–15 h prior to I) protects the liver from warm I/R injuryInduction of heme oxygenase-1 and inhibition of cytochrome P450 2E1[178]

Hepatic I/R in vivo (mice)Na2S (1 mg/kg, 5 min prior to R) protects the murine liver against I/R injuryUpregulation of intracellular antioxidant and antiapoptotic signaling pathways[179]

Hepatic I/R in vivo (mice)H2S (100 ppm, 5 min prior to R) protects the liver against I/R injuryReduction of necrosis, apoptosis, and inflammation[180]

Hepatic I/R in vivo (mice)NaHS (14 and 28 μM/kg, 30 min prior to I) attenuates hepatic I/R injuryWeaken the apoptosis through the inhibition of c-Jun N-terminal protein kinase 1 signaling pathway[181]

Hepatic I/R in vivo (rat)NaHS (12.5, 25 and −50 μM/kg, 5 min prior to I) reduces liver damage after perioperative I/R injuryInhibition of mitochondrial permeability transition pore opening, reduction of cell apoptosis, and activation of Akt-GSK-3β signaling[182]