Objective:To investigate the role of plasminogen activator inhibitor-1 (PAI-1) in the development and spontaneous regression of liver fibrosis. Methods:Rat liver fibrosis models were induced by subcutaneous injection of carbon tetrachloride(CCl4) and tissue samples were obtained for study at various times. The different stages of fibrosis were confirmed with HE and VG staining,and then the expression of PAI-1 in these tissue samples was detected by reverse transcription polymerase chain reaction (RT-PCR) and immunohistochemistry. Results:There was only weak expression of PAI-1 detected in endochylema located in portal area of normal liver,and the expression of PAI-1 was mainly located within the area of hepatic sinusoid and endochylema in fibrotic liver. The PAI-1 expression increased accordingly with the development and progression of fibrosis while decreased in spontaneous regression. Semiquantitative analysis showed that the expression of PAI-1 for normal control and 2,4,6 weeks after CCl4 administration were 0.142 ± 0.030,0.361 ± 0.048,0.757 ± 0.068 and 0.838 ± 0.048,the expression of PAI-1 for 2,4,6 weeks after resolution of fibrosis were 0.613 ± 0.054,0.524 ± 0.060 and 0.210 ± 0.044. Semiquantitative analysis by RT-PCR showed that the mRNA expression of PAI-1 in the model group treated with CCl4 for 2,6,8 weeks was higher than that in normal control,increasing to 6.83 ± 2.60,12.43 ± 2.65 and 26.32 ± 5.17 fold. Nevertheless,the mRNA expression of PAI-1 decreased with the resolution of fibrosis after stopping CCl4 induction. The mRNA expression of PAI-1 for 2,4,6 weeks after resolution of fibrosis was 17.86 ± 4.6,14.62 ± 5.99 and 11.21 ± 1.98 times,respectively,compared with normal control. Conclusion:PAI-1 was up-regulated in liver fibrosis development while down-regulated in spontaneous regression,which indicated that it may play an important role in the development and progression of hepatic fibrosis.