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Experimental models | Effects | Proposed mechanisms | References |
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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] |
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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] |
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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] |
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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] |
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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] |
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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] |
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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] |
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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] |
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