title: The antioxidant EPC-K1 attenuates renal ischemia-reperfusion injury in a rat model.
abstract: BACKGROUND
  Acute kidney injury (AKI) occurs frequently in the intensive care unit. A primary cause is renal ischemia/reperfusion (I/R) injury, during which excess reactive oxygen species (ROS) are produced. ROS subsequently damage renal cells, leading to the development of AKI. Here, we investigated whether renal I/R injury could be attenuated by the antioxidant EPC-K1.
  
  
  METHODS
  We divided male Wistar rats into the following three groups: (1) a renal I/R group, (2) an EPC-K1 + renal I/R group and (3) a control group. Rats were sacrificed 24 h after treatment (I/R or sham). To measure oxidative stress in renal tissue, histological examinations were performed and serum levels of blood urea nitrogen (BUN) and creatinine were measured. The antioxidant action of EPC-K1 was also evaluated in RAW264.7 cells stimulated with antimycin A.
  
  
  RESULTS
  Serum BUN and creatinine levels were elevated in the I/R group; however, this increase was significantly attenuated by EPC-K1 in the EPC-K1 + I/R group. Renal tissue injury was also significantly lower in the EPC-K1 + I/R group compared with the I/R group. In vitro experiments showed that EPC-K1 significantly attenuated the generation of ROS induced by antimycin A.
  
  
  CONCLUSIONS
  In our study, EPC-K1 was able to attenuate AKI due to renal I/R by reducing oxidative stress. These results suggest that EPC-K1 may be effective against various types of I/R injury.
authors.affiliation: Department of Anesthesiology and Intensive Care Medicine, Oita University Faculty of Medicine, Yufu City, Japan. kamome@oita-u.ac.jp
authors.forename: Shunsuke
authors.initials: S
authors.lastname: Yamamoto
authors.forename: Satoshi
authors.initials: S
authors.lastname: Hagiwara
authors.forename: Seigo
authors.initials: S
authors.lastname: Hidaka
authors.forename: Chihiro
authors.initials: C
authors.lastname: Shingu
authors.forename: Koji
authors.initials: K
authors.lastname: Goto
authors.forename: Kenji
authors.initials: K
authors.lastname: Kashima
authors.forename: Takayuki
authors.initials: T
authors.lastname: Noguchi
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000627:therapeutic use*; D001205:Ascorbic Acid / Q000031:analogs & derivatives* / Q000627:therapeutic use; D015415:Biomarkers / Q000097:blood; D002460:Cell Line; D004195:Disease Models, Animal; D007668:Kidney / Q000098:blood supply* / Q000648:ultrastructure; D007674:Kidney Diseases / Q000097:blood / Q000473:pathology / Q000517:prevention & control*; D007677:Kidney Function Tests; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D051379:Mice; D018384:Oxidative Stress; D051381:Rats; D017208:Rats, Wistar; D017382:Reactive Oxygen Species / Q000378:metabolism; D015427:Reperfusion Injury / Q000097:blood / Q000473:pathology / Q000517:prevention & control*; D014810:Vitamin E / Q000031:analogs & derivatives* / Q000627:therapeutic use
chemical_list: D000975:Antioxidants; D015415:Biomarkers; D017382:Reactive Oxygen Species; D014810:Vitamin E; D008315:Malondialdehyde; C066638:potassium ascorbyl tocopheryl phosphate; D001205:Ascorbic Acid