Protective action of D-ribose against renal injury caused by ischemia and reperfusion in rats with transient hyperglycemia.

Hyperglycemia amplifies the inflammatory state after ischemia/reperfusion (I/R), and activated neutrophils have been implicated in the development of I/R-induced renal injuries. D-ribose is a naturally occurring monosaccharide found in all living cells. In this study, we examined whether D-ribose attenuates I/R-induced renal injury by reducing neutrophil activation in rats with transient hyperglycemia. Male Wistar rats were divided into sham (n = 24), control (n = 64), and D-ribose (n = 32) groups. Rats received intraperitoneal injection of glucose (3 g/kg) 30 min before induction of ischemia to induce transient hyperglycemia. Anesthetized rats underwent right nephrectomy and subsequent occlusion of the left renal artery and vein for 45 min. D-ribose (400 mg/kg) was intravenously administered 30 min before induction of ischemia. D-ribose significantly reduced the degree of the I/R-induced increases in renal concentrations of cytokine-induced neutrophil chemoattractant-1 (a chemotactic factor for the activation of neutrophils and chemotaxis to the site of injury) and myeloperoxidase (an indicator of neutrophils infiltration). D-ribose also reduced the I/R-induced increases in serum levels of blood urea nitrogen and creatinine, and improved histological changes, including acute tubular necrosis in the corticomedullary junction fields. These results indicate that D-ribose reduces the I/R-induced acute renal injury in rats with transient hyperglycemia, probably by reducing neutrophil activation. D-ribose might thus be useful for surgical procedures, such as renal transplant surgery, under hyperglycemia.