Table 4.

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

Experimental models	Effects	Proposed mechanisms	References
Hepatic I/R in vivo (rat)	NaHS (28 μM/kg, prior to R) attenuates the injured hepatic function and the synthetic action of hepatocytes	Inhibition 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 injuries	Activation 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 peroxidation	Antioxidant 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 injury	Induction 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 injury	Upregulation 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 injury	Reduction 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 injury	Weaken 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 injury	Inhibition of mitochondrial permeability transition pore opening, reduction of cell apoptosis, and activation of Akt-GSK-3β signaling	[182]