Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2002-9-9
pubmed:abstractText
Heme oxygenase-1 (HO-1) is an antioxidant enzyme and is believed to protect against oxidative stress-induced tissue injury. Renal ischemia-reperfusion (IR) injury seems at least in part to be caused by the oxidative stress. The aim of this study was to improve the renal IR injury by clinically available means. When littermate hemolysate was intravenously administered into rats, HO-1 was markedly induced in the kidneys. To investigate whether prior induction of HO-1 by the hemolysate injection ameliorates the subsequent renal IR injury, we assessed the levels of blood urea nitrogen (BUN) and serum creatinine (SCr), markers for renal injury, in rats with 45 min of ischemia followed by 18 h of reperfusion. To avoid the nephrotoxicity induced by hemolysate, small but effective amounts of hemolysate was injected into rats at 48 h prior to the ischemia. The levels of BUN and SCr values were significantly improved as compared to the rats with renal IR injury alone. Administration of HO inhibitor abolished the efficacy of hemolysate pretreatment. Our findings indicated that the prior induction of HO-1 by treatment of littermate hemolysate ameliorated the subsequent renal IR injury. Prior injection of self-hemolysate would be clinically useful for the protection against the renal IR injury induced by kidney transplantation and kidney surgery without immunological and infectious problems.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0028-2766
pubmed:author
pubmed:copyrightInfo
Copyright 2002 S. Karger AG, Basel
pubmed:issnType
Print
pubmed:volume
92
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
407-13
pubmed:dateRevised
2005-11-17
pubmed:meshHeading
pubmed:year
2002
pubmed:articleTitle
Hemolysate pretreatment ameliorates ischemic acute renal injury in rats.
pubmed:affiliation
Department of Pathological Biochemistry, Medical Research Institute, Tokyo Medical and Dental University, 2-3-10 Kanda-surugadai, Chiyoda-ku, Tokyo 101-0062, Japan.
pubmed:publicationType
Journal Article