Review Article

Hydrogen Sulfide as a Novel Regulatory Factor in Liver Health and Disease

Table 2

Protective effects of H2S on hepatic I/R injury.

Experimental modelsEffectsProposed mechanismsRefs.

Hepatic I/R in vivo (rat)NaHS (14 μM/kg, 30 min prior to I) attenuates the severity of liver injury and inhibits the production of lipid peroxidation, serum inflammatory factors, and apoptosis-related proteinsAntioxidant and antiapoptotic activities[21]
Hepatic I/R in vivo (mouse)H2S (100 ppm, 5 min prior to R) protects the liver against I/R injuryReduction of apoptosis, necrosis, and inflammation[119]
Hepatic I/R in vivo (rat)GYY4137 (an H2S donor, 133 μM/kg, 1 h prior to I) attenuates the reduced cell viability and the increased apoptosis induced by hepatic I/RActivation of the Akt pathway regulated by miR-21[120]
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 MPTP opening and the activation of Akt-GSK-3β signaling[121]
Hepatic I/R in vivo (rat)NaHS (20 μM/kg, 30 min prior to I) reduces hepatic I/R injury in the young ratsActivation of the Nrf2 signaling pathway[122]
Hepatic I/R in vivo (rat)NaHS (5 mg/kg/d for 11 days) protects against cognitive impairment in rats undergoing hepatic I/RReduction of neuroinflammation in the hippocampus[123]
Hepatic I/R in vivo (mouse)NaHS (1 mg/kg prior to R) ameliorates hepatic I/R injury by direct and indirect antioxidant activities and by accelerating hepatic regenerationVia mechanisms involving Nrf2 and Akt-p70S6k[124]
Hepatic I/R in vivo (rat)NaHS (5 mg/kg/d for 11 days) exerts a protective effect on hepatic I/R-induced cognitive impairmentMay be associated with the NR2B subunit of the NMDA receptors[125]
Hepatic I/R in vivo (mouse)NaHS (1.5 mg/kg, 1 h prior to I) protects against hepatic I/R injuryPartly through AKT1 activation[126]
Hepatic I/R in vivo (mouse)NaHS (14 and 28 μM/kg, 30 min prior to I) attenuates hepatic I/R injuryPartly through regulation of apoptosis via inhibiting JNK1 signaling[127]
Hepatic I/R in vivo (rat)NaHS (28 μM/kg, prior to R) attenuates hepatic I/R-induced renal and cardiac injuryReduction of myocardial and renal inflammation and oxidative potential[128]
Hepatic I/R in vivo (mouse)Na2S (an H2S donor, 1 mg/kg, 5 min prior to R) protects the murine liver against I/R injuryUpregulation of intracellular antioxidant and antiapoptotic signaling pathways[30]

MPTP: mitochondrial permeability transition pore; GSK-3β: glycogen synthase kinase-3 beta; Nrf2: nuclear factor erythroid 2-related factor 2; NMDA: NR2B subunit of N-methyl-D-aspartate; JNK1: c-Jun N-terminal kinase 1.