|
| Experimental models | Effects | Proposed mechanisms | References |
|
| Renal I/R in vivo (mice) | NaHS (1 mg/kg, 15 min prior to I) rescues mice from the injury and mortality | Modulation of oxidative stress | [14] |
|
| Renal I/R in vivo (mice) | H2S (100 ppm, before and after treatment) shows protective effects on survival, renal function, apoptosis, and inflammation | A hypometabolic state induced by H2S | [183] |
|
| Renal I/R in vivo (pig) | Na2S (100 µg/kg, 10 min prior to R) results in a marked reduction in kidney injury and preserves glomerular function | Anti-inflammatory effects | [184] |
|
| Isolated perfused kidney ex vivo (pig) | H2S (0.5 mM, 10 min before and after R) ameliorates the renal dysfunction | Activation of KATP channels | [185] |
|
| Renal I/R in vivo (mice) | NaHS (100 µM/kg, 30 min prior to I) significantly attenuates I/R injury-induced renal dysfunction | The increase in expression of CSE | [186] |
|
| Renal I/R in vivo (rat) | NaHS (100 µM/kg, 15 min prior to I and 5 min prior to R) attenuates renal I/R injury | Antiapoptotic and anti-inflammatory effects | [187] |
|
| Warm renal I/R in vivo (rat) | NaHS (150 µM, at time of renal pedicle clamping and during R) improves long-term renal function and decreases long-term inflammation | Antiapoptotic and anti-inflammatory effects | [188] |
|
| Warm renal I/R in vivo (rat) | NaHS (150 µM, during I and R) increases renal capillary perfusion and improves acute tubular necrosis and apoptosis | Decrease of leukocyte migration and inflammatory responses | [189] |
|
| Renal I/R in vivo (pig) | Na2S (2 mg/kg, 2 h prior to I) attenuates tissue injury and organ dysfunction | Antioxidant and anti-inflammatory effects | [190] |
|
| Renal I/R in vivo (rat) | NaHS (100 µg/kg, 20 min prior to I or 10 min prior to R) protects against renal I/R injury | Antioxidant and antiapoptotic effects | [191] |
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