Table 5.

Effects of H₂S and its donors in renal I/R injury.

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]