title: D-ribose attenuates ischemia/reperfusion-induced renal injury by reducing neutrophil activation in rats.
abstract: The ischemia/reperfusion (I/R) represents a common pathological mechanism that causes renal injuries. A monosaccharide D-allose has been shown to inhibit neutrophil activation, which is involved in the I/R-induced organ injuries. We therefore examined the role of D-ribose in the I/R-induced renal injury using a rat model. D-ribose, a monosaccharide found in all living cells, serves as a key component of adenosine-5'-triphosphate and nicotinamide adenine dinucleotide. Male Wistar rats were divided into the sham, control and D-ribose groups. In the control and D-ribose groups, rats were subjected to 45 min of left renal ischemia, followed by 24 h of reperfusion, while the I/R procedure was not performed in the sham group. Rats were intravenously administered D-ribose (sham group and D-ribose group, 400 mg/kg) or saline (control group) 30 min before ischemia. Blood urea nitrogen (BUN), serum creatinine and urinary N-acetyl beta-D-glucosaminidase (NAG) were measured as indicators of glomerular function and proximal tubular function. We also measured cytokine-induced neutrophil chemoattractant-1 (CINC-1) and myeloperoxidase concentrations to assess neutrophil activation and infiltration, respectively. The tissue sections were scored to evaluate the tubular injury. In the control group, BUN, creatinine, NAG, CINC-1, myeloperoxidase, histological severity score, and number of infiltrating neutrophils were increased following I/R insult, as compared with the sham group. Such increases in biochemical markers, severity score, and infiltrating neutrophils were significantly inhibited in the D-ribose group. Thus, D-ribose ameliorates the I/R-induced renal injury probably by inhibiting neutrophil activation, and may be useful in attenuating the renal injury associated with renal ischemia.
authors.affiliation: Department of Anesthesia and Perioperative Medicine, Kobe University Hospital, Kobe, Japan.
authors.forename: Hitoaki
authors.initials: H
authors.lastname: Sato
authors.forename: Masaaki
authors.initials: M
authors.lastname: Ueki
authors.forename: Takehiko
authors.initials: T
authors.lastname: Asaga
authors.forename: Kousuke
authors.initials: K
authors.lastname: Chujo
authors.forename: Nobuhiro
authors.initials: N
authors.lastname: Maekawa
mesh_terms: D000818:Animals; D054360:Chemokine CXCL1 / Q000378:metabolism; D007668:Kidney / Q000378:metabolism / Q000473:pathology*; D008297:Male; D018375:Neutrophil Activation / Q000502:physiology*; D009504:Neutrophils / Q000166:cytology / Q000378:metabolism*; D009195:Peroxidase / Q000378:metabolism; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D015427:Reperfusion Injury / Q000097:blood / Q000473:pathology*; D012266:Ribose / Q000378:metabolism*
chemical_list: D054360:Chemokine CXCL1; C513297:Cxcl1 protein, rat; D012266:Ribose; D009195:Peroxidase