Hepatocyte apoptosis induced by hepatic ischemia-reperfusion injury in cirrhotic rats.
OBJECTIVE
To investigate whether hepatocyte apoptosis in hepatic ischemia-reperfusion (I/R) injury is mediated by Fas pathway.


METHODS
Fas-mRNA expression detected by in situ hybridization assay, caspase-3 activity measured by fluorescence spectrophotometer, and hepatocyte apoptosis detected by TUNEL assay were compared in different I/R conditions between cirrhotic and normal rats. The relationship was analyzed between hepatocyte apoptosis, Fas-mRNA expression, and caspase-3 activity.


RESULTS
In cirrhotic rats, Fas-mRNA expression and caspase-3 activity were significantly increased when the ischemic time prolonged, and subsequently, hepatocyte apoptosis was increased (P<0.01). Under the same I/R condition, the Fas-mRNA expression, caspase-3 activity and hepatocyte apoptosis in cirrhotic liver were significantly higher than those in normal liver (P<0.01).


CONCLUSIONS
Hepatocyte apoptosis in hepatic I/R injury might be mediated by Fas pathway. The possible underlying mechanism that cirrhotic liver is more sensitive to ischemic injury than normal liver is alteration of Fas expression level.
Li
Shao-Qiang
SQ
Departments of Hepatobiliary Surgery, First Affi-liated Hospital, Zhongshan University, Guangzhou 510080, China. lesqch@yahoo.com.cn
Liang
Li-Jian
LJ
Huang
Jie-Fu
JF
Li
Zhi
Z
D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D053148:Caspase 3; D020169:Caspases / Q000096:biosynthesis; D022781:Hepatocytes / Q000502:physiology*; D008099:Liver / Q000098:blood supply / Q000503:physiopathology; D008103:Liver Cirrhosis / Q000150:complications / Q000503:physiopathology*; D008107:Liver Diseases / Q000503:physiopathology*; D051381:Rats; D015427:Reperfusion Injury / Q000150:complications / Q000503:physiopathology*; D015398:Signal Transduction; D019014:fas Receptor / Q000096:biosynthesis*
D019014:fas Receptor; C505410:Casp3 protein, rat; D053148:Caspase 3; D020169:Caspases