Table 1.
Summary of the protective effects of exogenous H2S ischemic treatment and post-treatment in animal models of cold and warm IRI.
| Model | H2S Treatment Modality | Effect of H2S | References |
|---|---|---|---|
| Warm cerebral IRI in mice | STS administered one minute or one minute and daily for one week after reperfusion | -Improved survival -Improved neurological function |
[43] |
| Warm hepatic IRI in mice | Na2S administered during ischemia (five minutes before reperfusion) | -Reduced liver injury -Increased ratio of GSH to GSSG -Increased protein expression of Trx-1, HSP-90, and Bcl-2 -Decreased protein expression of cleaved caspase-3 -Reduced lipid peroxidation |
[44] |
| Warm intestinal IRI in mice | NaHS administered during reperfusion | -Increased mesenteric perfusion -Reduced intestinal mucosal damage -Decreased levels of IL-6, IL-9, IL-10, VEGF, FGF-2, MIP-1α, eotaxin, IP-10, MIP-2, G-CSF, KC in intestinal tissue -Effects of H2S mediated through endothelial nitric oxide synthase |
[45] |
| Warm myocardial IRI in mice | Na2S administered during reperfusion | -Reduced myocardial injury and infarct size -Reduced level of IL-1β and apoptosis in cardiac tissue -Increased cardiac function -Reduced leukocyte infiltration -Increased efficiency of ETC complexes I and II |
[46] |
| Cold pancreatic IRI in pigs | AP39 administered during ischemia (preservation solution supplemented with AP39) | -Decreased ROS production -Increased mitochondrial membrane polarization -Increased ATP production -Decreased expression of IL-1β and TNF-α -Improved islet function in recipient mice following xenogeneic transplantation |
[47] |
| Cold pulmonary IRI in rabbits (ex vivo) | NaHS administered during reperfusion | -Decreased ROS production | [48] |
| Cold renal IRI in rats | NaHS administered during ischemia (preservation solution supplemented with NaHS) | -Improved recipient survival and renal function -Reduced renal tissue apoptosis and necrosis -Reduced leukocyte infiltration and expression of IFN-γ and ICAM-1 |
[49] |
| Warm renal IRI in mice | NaHS administered daily beginning two days after reperfusion | -Reduced renal tubule damage -Improved renal function and recovery of recipient body weight -Increased tubular epithelial cell and decreased interstitial cell proliferation -Reduced renal fibrosis -Decreased ROS production, ratio of GSSG to GSH, and Nox4 expression -Increased MnSOD and catalase expression |
[50] |
| Warm renal IRI in rats | AP39 administered during ischemia | -Improved renal function -Decreased ROS production -Decreased neutrophil infiltration and IL-12 levels -Decreased apoptosis |
[51] |
| Cold renal IRI in rats | STS administered during ischemia (preservation solution supplemented with STS) | -Improved recipient survival and renal function -Decreased apoptosis and necrosis -Decreased KIM-1, IFN-γ, TNF-α, IL-6, Bax, Caspase-3, and JNK2 expression -Increased PGC-1α, NDUFB8, SDHB, ERK1, and ERK2 expression -Decreased macrophage and neutrophil infiltration |
[15] |
| Cold renal IRI in rats | AP39 administered during ischemia (preservation solution supplemented with AP39) | -Improved recipient survival and renal function | [52] |
GSH: reduced glutathione; GSSG: oxidized glutathione; Trx-1: thioredoxin-1; 90-kDa heat shock protein (HSP-90); Bcl-2: B-cell lymphoma-2; IL-6: interleukin-6; IL-9: interleukin-9; IL-10: interleukin-10; VEGF: vascular endothelial growth factor; FGF-2: fibroblast growth factor 2; MIP-1α: macrophage inflammatory protein-1 alpha; IP10: C-X-C ligand 10; MIP-2: macrophage inflammatory protein 2; G-CSF: granulocyte-colony stimulating factor; KC: C-X-C ligand 1; IL-1β: interleukin-1 beta; ETC: electron transport chain; ROS: reactive oxygen species; ATP: adenosine triphosphate; TNF-α: tumor necrosis factor-alpha; IFN-γ: interferon gamma; ICAM-1: intercellular adhesion molecule-1; Nox4: NADPH oxidase 4; MnSOD: manganese superoxide dismutase; IL-12: interleukin-12; KIM-1: kidney injury molecule-1; Bax: Bcl-2 associated X-protein; JNK2: c-Jun N-terminal kinase 2; PGC-1α: Pparg coactivator 1 alpha; NDUFB8: NADH dehydrogenase [ubiquinone] 1 beta subcomplex subunit 8; SDHB: succinate dehydrogenase [ubiquinone] iron-sulfur subunit; ERK1: mitogen-activated protein kinase 1; ERK2: mitogen-activated protein kinase 2.