An insight into the protection of rat liver against ischemia/reperfusion injury by 2-selenium-bridged beta-cyclodextrin.
OBJECTIVE
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.


CONCLUSIONS
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.
Lin
Ting-Ting
TT
Key laboratory for Molecular Enzymology and Engineering of the Ministry of Education, Jilin University, Changchun, China.
Wang
Bing-Mei
BM
Li
Xin-Yang
XY
Pan
Yu
Y
Wang
Wei
W
Mu
Ying
Y
Liu
Jun-Qiu
JQ
Shen
Jia-Cong
JC
Luo
Gui-Min
GM