Inhibitory effect of miR-155 on expression of hepatitis B virus and its mechanism

Objective　To investigate the mechanism of miR-155 regulating SOCS1 in the inhibition of HBsAg and HBeAg. Methods　The pre-miR-155 was amplified from total DNA of HepG2.2.15 by PCR . The target gene fragment was digested and cloned into the pmR-mCherry plasmid. PmiR-155 was transfected into HepG2.2.15 cells (recombinant group) by liposome-mediated method. The empty plasmid, the reagent group and untreated cells were set as control. Firstly the expression of miR-155 was detected by the real-time quantitative PCR. Secondly, the expression of SOCS1 mRNA was detected by RT-PCR, and then the expression of SOCS1 protein was determined by Western blotting. Finally, the expression of HBsAg and HBeAg was determined by ELISA. Results　The pmiR-155 eukaryotic over-expression vector was successfully constructed. MiR-155 level of HepG2.2.15 cells which was transfected with the recombinant plasmid (519.43±52.10) was obviously higher than those of the empty plasmid (24.24±16.70) and reagent groups (35.04±26.09, P<0.05). RT-PCR showed the expression of SOCS1 mRNA was lower in recombinant group than in untreated group. The expression of SOCS1 protein markedly decreased as shown with Western blotting. Over-expression of miR155 could inhibit the expressions of HBsAg and HBeAg (55.62±3.77)% and (47.87±2.46)% (P<0.01) respectively. Conclusions　Over-expression of miR-155 can down regulate the expression of SOCS1, and inhibit the expressions of HBsAg and HBeAg. DOI: 10.11855/j.issn.0577-7402.2015.11.09