Effect of Hydrogen Sulfide on Kidney Injury in Rat Model of Crush Syndrome.

BACKGROUND

Acute kidney injury is the most serious complication of crush syndrome. Hydrogen sulfide (H2S) is an endogenously produced gaseous signaling molecule. It is involved in homeostatic functions, such as blood pressure control, apoptosis, oxidative stress, and inflammation. In this study, effects of H2S on kidney injury were investigated in a rat model of crush syndrome.

METHODS

Rats were divided into six groups (n = 8): Sham (steril saline ip), crush (sterile saline ip), crush + NaHS (sodium hydrosulfide, an H2S donor) (100 μmol/kg ip). All these groups were also separated as 3 and 24 h after decompression. Crush injury was induced by 6 h of direct compression to both hindlimbs of anesthetized rats with blocks weighing 3.6 kg each sides, followed by 3 or 24 h of decompression. Kidney injury molecule-1, neutrophil gelatinase-associated lipocalin, tumor-necrotizing factor-α, transforming growth factor-β, tissue total oxidant status, and total antioxidant status levels were measured in kidney homogenates 3 and 24 h after decompression. Serum creatine kinase, blood urea nitrogen, and creatinine levels were also measured. Apoptosis was assessed by TUNEL method. Bcl-2 was assessed by immunohistochemistry. Glomerular and tubular structures were also examined histopathologically.

RESULTS

NaHS reduced kidney injury molecule-1, neutrophil gelatinase-associated lipocalin, tumor-necrotizing factor-α, transforming growth factor-β, total oxidant status levels, and increased total antioxidant status levels in kidney 3 and 24 h after decompression. Serum urea, creatinine, and creatine kinase levels also reduced with NaHS. NaHS decreased renal damage and apoptosis in crush-related acute kidney injury.

CONCLUSIONS

These results suggest that H2S could reduce crush-related acute kidney injury via anti-inflammatory, antioxidant, and antiapoptotic effects.