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| Hepatocyte apoptosis induced by Hepatic ischemia-reperfusion injury in cirrhotic rats |
| Shao-Qiang Li, Li-Jian Liang, Jie-Fu Huang and Zhi Li |
Guangzhou, China
From the Departments of Hepatobiliary Surgery (Li SQ, Liang LJ and Huang JF) and Pathology (Li Z), First Affi-liated Hospital, Zhongshan University, Guangzhou 510080, China
Correspondence: Shao-Qiang Li, MD (Tel: 86-20-87755766ext8096; Fax: 86-20-87755766ext8663; Email: lesqch@yahoo.com.cn) |
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Abstract 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.
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2003, Vol. 2 
