The Expression Of TGF-β1,TβR And Smad2/3 In Liver Of Mice Infected With Echinococcus Multilocularis

Objective:To systemically and dynamically observe the expression of TGF-P 1, TGF-β1 receptors (TβRⅠ, TβRⅡ) and Smad2/3 in the liver of Balb/c mice infected by Echinococcus multilocularis (Em), the level of liver fibrosis and pathological alteration to be demonstrated, further the mechanism in the development of liver alveolar echinococcosis to be revealed. Methods:Balb/c mice were randomly allocated into an experiment group and an normal control group, to get the tissue of liver systemically and dynamically. The mRNA of TGF-β1, TβR, Smad2 and Smad3 were analyzed by RT-PCR, the protein expression and location of TGF-β1Ⅰ, TβRⅡand Smad2/3 were analyzed by Western-blot and immuhistochemistry respectively. The level of liver fibrosis and pathological alteration were observed by HE and Massion staining. Results:1) Balb/c mice infected by Em at 8 weeks after infection, some alveclar sphereuesicae could be observed obviously and be found everywhere at 24 weeks after infection.2) RT-PCR demonstrated that the expression of TGF-β1 mRNA increased gradually infected by Em at 8 weeks after infection. The expression of Smad3 mRNA at every time of control group was all lower than experiment group beside 2 days and 36 weeks.3) The level of expression of protein TGF-β1 increased gradually at 8 weeks after infection, peak at 12 weeks. The level of expression of protein Smad2/3 was lower in infected mice than the control group, but it's expression increased gradually after 8 days, peak at 4 weeks, then decreased gradually.4) TGF-β1, TβRⅠ, TβRⅡ, Smad2/3 only observed in hepatic sinusoid in the control group, while in hepatic sinusoid, hyalomitome, cell membrane, fiber organization, focus germinal layer surrounding in infected group. TGF-β1 reached peak at 12 weeks but TβRⅡpeak at 24 weeks. The expression of Smad2/3 and TβRⅠwas all reached peak at 8 weeks.5) In the different Em infected time, the inflammation and fibrosis were observed in the liver of infected group. Conclusion:The pathway of TGF-β/ Smads signal protein activated in Balb/c mice infected by Em to participate the liver fibrosis and hepatic injury possibly. The TGF-β/Smads signal transduction pathway may be mediated the expression of TGF-β1.