title: The vitamin E derivative, ESeroS-GS, attenuates renal ischemia-reperfusion injury in rats.
abstract: BACKGROUND
  Acute kidney injury (AKI), which occurs during renal transplantation and cardiovascular surgery, is a major clinical problem associated with high mortality, and has limited treatment options. Anti-inflammation therapy has been suggested to improve the course and outcome of AKI. In this study, we hypothesized that ESeroS-GS, a vitamin E derivative, inhibits cytokine production and prevents renal ischemia-reperfusion (I/R) injury in rats.
  
  
  METHODS
  Rats received an intravenous infusion of ESeroS-GS or saline, and underwent experimentally-induced renal I/R injury or sham treatment. Rats were sacrificed after 60 min of ischemia and 24 h of reperfusion. To evaluate the renal protective effects of ESero-GS, renal function was examined, kidneys were histologically assessed, levels of myeloperoxidase (MPO) and serum cytokines were measured, and caspase 3/7 activity was determined.
  
  
  RESULTS
  ESeroS-GS attenuated I/R-induced histologic alterations, reduced levels of MPO and serum BUN, Cre, TNF-α, and IL-6, and decreased caspase 3/7 activity in kidneys of rats subjected to renal I/R injury.
  
  
  CONCLUSIONS
  ESeroS-GS attenuated renal injury after I/R by reducing serum cytokine levels. Our findings suggest that ESeroS-GS may have therapeutic potential against various human I/R conditions.
authors.affiliation: Department of Anesthesiology and Intensive Care Medicine, Oita University Faculty of Medicine, Yufu City, Oita, Japan.
authors.forename: Hironori
authors.initials: H
authors.lastname: Koga
authors.forename: Satoshi
authors.initials: S
authors.lastname: Hagiwara
authors.forename: Hideto
authors.initials: H
authors.lastname: Mei
authors.forename: Nozomi
authors.initials: N
authors.lastname: Hiraoka
authors.forename: Jyunya
authors.initials: J
authors.lastname: Kusaka
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; D001578:Benzopyrans / Q000737:chemistry / Q000494:pharmacology* / Q000627:therapeutic use*; D001806:Blood Urea Nitrogen; D053148:Caspase 3 / Q000378:metabolism; D053179:Caspase 7 / Q000378:metabolism; D007211:Indoles / Q000737:chemistry / Q000494:pharmacology* / Q000627:therapeutic use*; D015850:Interleukin-6 / Q000097:blood; D007668:Kidney / Q000098:blood supply* / Q000187:drug effects* / Q000378:metabolism; D008297:Male; D023421:Models, Animal; D009195:Peroxidase / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D015427:Reperfusion Injury / Q000517:prevention & control*; D014409:Tumor Necrosis Factor-alpha / Q000097:blood; D014810:Vitamin E
chemical_list: D001578:Benzopyrans; D007211:Indoles; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha; C475739:glutamyl-(2-(((3,4-dihydro-2,5,7,8-tetramethyl-2-(4,8,12-trimethyltridecyl)-2H-1-benzopyran-6-yl)oxy)carbonyl)-3-((2-(1H-indol-3-yl)ethyl)amino)-3-oxopropyl)-cysteinyl-glycine sodium salt; D014810:Vitamin E; D009195:Peroxidase; D053148:Caspase 3; D053179:Caspase 7