The effects of interleukin-10 on the expression of Fas and FasL in rat hepatic stellate cells.
OBJECTIVE
To study the effects of interleukin-10 on the expression of fas and fasL in hepatic stellate cells in experimental rat hepatic fibrosis.


METHODS
Sixty clean SD rats were divided into control group (8 in group N), the model group (28 in group C) and the IL-10 treated group (24 in group I) randomly. The rats were administered CCl4 with or without IL-10 treatment. Hepatic stellate cells (HSCs) were isolated from these rats at the beginning of the seventh and eleventh weeks during the course of liver fibrosis, respectively. Semi-quantitative RT-PCR and Western-blot were used to analyze mRNA and protein expressions of Fas and FasL from freshly isolated HSC. The liver tissues were harvested from three groups.


RESULTS
The CCl4- induced experimental rat hepatic fibrosis model was established successfully. The IL-10 could decrease the fibrotic degree of rat liver. The Fas and FasL mRNA can be measured in HSC of 3 groups. The mRNA of Fas and FasL in group C were significantly increased time-dependently compared to those of control group. In the 7th week, the expression level of Fas and FasL in group C was 0.66+/-0.02 and 0.45+/-0.33 respectively, and in the group I, the level was 0.74+/-0.02 and 0.52+/-0.05 respectively. In the 11th week, the level in group C was 0.72+/-0.02 and 0.62+/-0.04 respectively, and in the group I, the level was 0.73+/-0.04 and 0.83+/-0.04 respectively. The western-blot analysis showed that there was no FasL expression in group N, the expression of Fas and FasL in group C was significantly increased time-dependently compared to those of control group. After being treated with IL-10, the expression level of Fas and FasL was higher than those of group C. In group C, the expression level of Fas and in the 11th week was 0.92+/-0.02 and 0.99+/-0.02 respectively, and in group I, the level was 0.96+/-0.16 and 1.22+/-0.03 respectively. In group C, the level of FasL in the 7th week and in the 11th week was 1.24+/-0.03 and 1.33+/-0.03 respectively, and in group I, the level was 1.36+/-0.16 and 1.39+/-0.19 respectively.


CONCLUSIONS
The expression of Fas and FasL increased in the course of the liver fibrosis, and would be furthered by IL-10. The IL-10 could cause the apoptosis of activated HSC, and making antifibrogenic come into effect in these ways.
Zhang
Lijuan
L
Department of Gastroenterology, Union Hospital of Fujian Medical University, Fuzhou, Fujian, 350001 China.
Wang
Xiaozhong
X
Zheng
Weida
W
Shi
Meina
M
D000818:Animals; D002251:Carbon Tetrachloride; D053222:Fas Ligand Protein / Q000235:genetics*; D005786:Gene Expression Regulation / Q000187:drug effects; D016753:Interleukin-10 / Q000494:pharmacology*; D008099:Liver / Q000473:pathology*; D008103:Liver Cirrhosis / Q000139:chemically induced / Q000473:pathology*; D012333:RNA, Messenger / Q000032:analysis; D051381:Rats; D017207:Rats, Sprague-Dawley; D019014:fas Receptor / Q000235:genetics*
D053222:Fas Ligand Protein; C505658:Fasl protein, mouse; D012333:RNA, Messenger; D019014:fas Receptor; D016753:Interleukin-10; D002251:Carbon Tetrachloride