| Objective:To investigate the effect of total flavone of Litchi Chinensis Sonn (TFL)on the expression of TGF-β1,Smad3and Smad7of hepatic fibrosis in rats, and to explore anti-fibrotic mechanism of TFL. Methods:Eighty males SD rats were randomly divided into four groups:sham-operated group, bile duct ligation (BDL) group, BDL with high-dose TFL treatment group(200mg·kg-1·d-1), BDL with low-dose treatment group(100mg·kg-1·d-1). The liver fibrosis which was induced by common bile duct ligation in rat was used as the animal model for this study, whereas the sham-operated group was used as controls.The rats were sacrificed at2nd,3rd and4th week respectively after operation. Histopathological changes in liver were observed under light microscopy by Hematoxylin and Eosin (H&E) staining.The expression of TGF-β1,Smad3and Smad7in liver tissues was detected by immunohistochemistry. Results:Weak expression of TGF-β1and Smad3at2nd,3rd and4th week after operation was found in liver of sham-operated group while overexpression of Smad7at the same time point was observed. Compared with BDL group, treatment with high-dose TFL significantly prevented the development of BDL-induced hepatic fibrosis. With the development of fibrosis, the expression of TGF-β1(3.000±1.309、2.000±1.309、1.800±1.649)and Smad3(2.875±1.458、2.000±1.309、1.833±0.753) in BDL with high-dose TFL tratment group was decreased at2nd,3rd and4th week after operation,while the expression of Smad7(3.375±1.061、4.250±1.035、4.833±0.753) was gradually increased at the same time.There was significant difference between BDL group and BDL with high-dose TFL treatment group (P<0.01, P<0.05). The expression level of TGF-β1,Smad3and Smad7in liver tissue of BDL with lower-dose TFL treatment group was between BDL group and BDL with high-dose TFL treatment group. However, there is no significant difference compared with BDL group(P>0.05). Conclusion:High-dose TFL may effectively reduce liver injury and hepatic fibrosis in BDL rats.The protective effect of TFL may be mediated through the inhibition of the over-expression of TGF-β1and Smad3, and increased the expression of Smad7. |
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