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Expression of tissue-type plasminogen and plasminogen activator inhibitor-1 in liver of rats with nonalcoholic fatty liver disease

Objective To investigate the expression and possible roles of plasminogen activator inhibitor 1(PAI 1) and tissue type plasminogen activator (t PA) in liver of rats with nonalcoholic fatty liver disease(NAFLD). Methods To induce NAFLD model, a fat rich diet which is consisted of 10% lard oil and 2% cholesterol was given to Sprague Dawley rats for a period of 8, 12, 16 and 24 week, respectively. Another group of rats fed normal diet were taken as normal control. Hepatic injury were assessed by histopathology (H E and VG stain) according to the scoring system proposed by Brunt et al. The expression of message RNA of PAI 1 and t PA in the liver were detected by semi quantitative RT PCR. Results Simple fatty liver were observed in model group at 8 week. From 12 to 24 week, the liver progressed gradually from steatohepatitis to steatohepatitis associted with fibrosis.Semi quantitive RT PCR revealed that the up regulated expression of PAI 1 mRNA with time in the liver of rats with NAFLD, and mRNA expression of PAI 1 was peaked in 24 week compared to control group(1.02±0.11 vs 0.51 ±0.09 , P 0.01 ). A positive correlation was notable between the mRNA expression of PAI 1 and the severity of liver steatosis( r =0.492, P 0.01) and the histopathology score( r =0.372, P 0.05). On the other hand, hepatic t PA gene expressions in the model group decreased from the 8 week and continued to decrease over time compared with control, with the lowest levels at 24 week(0.89±0.11 vs 1.62±0.10, P 0.01), a negative correlation was only seen between the expression of mRNA of t PA and the histopathology score ( r =-0.368, P 0.05),but no significant correlation were found with the severity of liver steatosis. Conclusion Above results indicate that increased PAI 1 and decreased t PA expression in the liver of rats fed with fat rich diet could be involved in the pathogenesis of NAFLD.