title: ETS-GS, a new antioxidant, ameliorates renal ischemia-reperfusion injury in a rodent model.
abstract: BACKGROUND
  Ischemia-reperfusion (I/R) contributes to acute kidney injury (AKI). On the other hand, anti-oxidative drugs help to prevent renal injury caused by I/R. The current study examined whether a new antioxidant, ETS-GS, inhibits reactive oxygen species (ROS) generation and thereby prevents renal I/R injury in rodent models.
  
  
  METHODS
  Rats with experimentally-induced renal I/R injury were treated concurrently with an intravenous injection of either ETS-GS or saline. Anesthesia was induced with sevoflurane.
  
  
  RESULTS
  Histologic examination revealed marked reduction of interstitial congestion, edema, inflammation, and hemorrhage in kidney tissue harvested 24 h after ETS-GS treatment. Renal I/R-induced secretion of nitric oxide (NO) in serum was inhibited by ETS-GS treatment. Furthermore, malondialdehyde (MDA) levels in the kidney were significantly lower in ETS-GS-treated rats with renal I/R. Moreover, when murine macrophage-like RAW264.7 cells were stimulated with antimycin A in the presence or absence of simultaneous ETS-GS treatment, ETS-GS decreased ROS levels.
  
  
  CONCLUSIONS
  Thus, ETS-GS lowered ROS levels in cultured cells, reduced serum NO levels, decreased renal MDA levels, and protected rats against I/R-induced kidney injury. Given these in vitro and in vivo findings, ETS-GS is a strong candidate for future exploration of therapeutic potential in various human I/R diseases.
authors.affiliation: Department of Anesthesiology and Intensive Care Medicine, Oita University Faculty of Medicine, Oita, Japan. saku@med.oita-u.ac.jp
authors.forename: Satoshi
authors.initials: S
authors.lastname: Hagiwara
authors.forename: Hironori
authors.initials: H
authors.lastname: Koga
authors.forename: Hideo
authors.initials: H
authors.lastname: Iwasaka
authors.forename: Kyosuke
authors.initials: K
authors.lastname: Kudo
authors.forename: Akira
authors.initials: A
authors.lastname: Hasegawa
authors.forename: Jyunya
authors.initials: J
authors.lastname: Kusaka
authors.forename: Isao
authors.initials: I
authors.lastname: Yokoi
authors.forename: Takayuki
authors.initials: T
authors.lastname: Noguchi
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000737:chemistry / Q000494:pharmacology*; D001806:Blood Urea Nitrogen; D002460:Cell Line; D003404:Creatinine / Q000097:blood; D004195:Disease Models, Animal; D007668:Kidney / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D007674:Kidney Diseases / Q000188:drug therapy* / Q000378:metabolism* / Q000473:pathology; D008264:Macrophages / Q000166:cytology / Q000187:drug effects; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D051379:Mice; D009569:Nitric Oxide / Q000378:metabolism; D009842:Oligopeptides / Q000737:chemistry / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D017382:Reactive Oxygen Species / Q000378:metabolism; D015427:Reperfusion Injury / Q000188:drug therapy* / Q000378:metabolism* / Q000473:pathology; D015996:Survival Rate
chemical_list: D000975:Antioxidants; D009842:Oligopeptides; D017382:Reactive Oxygen Species; C568419:gamma-L-glutamyl-S-(2-(((3,4-dihydro-2,5,7,8-tetramethyl-2-(4,8,12- trimethyltridecyl)-2H-1-benzopyran-6-yl)oxy)carbonyl)-3-oxo-3-((2-sulfoethyl)amino)propyl)-L-cysteinylglycine sodium salt; D009569:Nitric Oxide; D008315:Malondialdehyde; D003404:Creatinine