Table 2.
Protective effects of H2S on hepatic I/R injury.
| Experimental models | Effects | Proposed mechanisms | Refs. |
|---|---|---|---|
| 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 proteins | Antioxidant and antiapoptotic activities | [21] |
| Hepatic I/R in vivo (mouse) | H2S (100 ppm, 5 min prior to R) protects the liver against I/R injury | Reduction 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/R | Activation 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 injury | Inhibition 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 rats | Activation 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/R | Reduction 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 regeneration | Via 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 impairment | May 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 injury | Partly 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 injury | Partly 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 injury | Reduction 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 injury | Upregulation 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.