An insight into the protection of rat liver against ischemia/reperfusion injury by 2-selenium-bridged beta-cyclodextrin.
Hepatol Res
; 39(11): 1125-36, 2009 Nov.
Article
in En
| MEDLINE
| ID: mdl-19624763
ABSTRACT
AIM:
The reperfusion following liver ischemia results in the damage and apoptosis of hepatocytes. The aim of this study was to investigate the possible effects and mechanism of a new synthesized glutathione peroxidase (GPX) mimic, 2-selenium-bridged beta-cyclodextrin (2-SeCD), on rat liver ischemia-reperfusion (I/R) injury.METHODS:
Male Wistar rats (n = 32) were randomly divided into four groups I. sham-operated group, II. I/R group, III. I/R +2-SeCD group, IV. I/R + Ebselen group. Hepatic I/R was administered by 90 min of ischemia and 12 h of reperfusion. Liver tissues were collected at the end of reperfusion period for measurement of various biochemical parameters.RESULTS:
The serum aspartate aminotransferase (AST), alanine aminotransferase (ALT) activity and tissue malondialdehyde, myeloperoxidase levels were increased in I/R group, while the increase was significantly reduced by 2-SeCD treatment. The glutathione level, depressed by I/R, was elevated back to normal levels by treatment with 2-SeCD. Severe hepatic damage were observed by light and transmission electron microscopy whilst pretreatment with 2-SeCD resulted in tissue and cellular preservation. Furthermore, 2-SeCD reduced cytochrome c release from mitochondria and subsequent DNA fragmentation by regulating Bcl-2/Bax expression ratio. RESULTS suggested that 2-SeCD was more effective than ebselen in the reversal of the alteration in tissue structural and biochemical parameters caused by I/R injury.CONCLUSION:
2-selenium-bridged beta-cyclodextrin playes an important role in the protection of liver against I/R injury and this treatment may be a novel pharmacological agent for liver surgery.
Full text:
1
Collection:
01-internacional
Database:
MEDLINE
Language:
En
Journal:
Hepatol Res
Year:
2009
Document type:
Article
Affiliation country:
China