Objective To investigate the effects of siRNA mediated HMGA 1 silence on proliferation and the gene expression of HMGA1 ,α-SMA and E-cadherin in activated hepatic stellate cells and its mechanisms .Methods Synthetic HMGA1 siRNA was transfected into LX-2 cells to silence the HMGA1 gene .The expression level of HMGA1 ,α-SMA and E-cadherin was determined by RT-PCR and Western blot experiments .LX-2 cell proliferation was assessed by M TT assay .Results The best inhibited effect was HMGA1-siRNA-1 .Compared with control group ,the cell proliferation and the mRNA and protein expression of HMGA 1 ,α-SMA in TGF-β1 group and TGF-β1 + NC-siRNA group were significantly increased (P< 0 .05) ,without significant differences between the two groups (P> 0 .05) ,while the expression of E-cadherin in TGF-β1 group and TGF-β1 + NC-siRNA group were significantly decreased compared with control group (P< 0 .05) .Meanwhile ,the cells in TGF-β1 + HMGA1 siRNA group showed significantly decreased proliferation level ,down-regulated mRNA and protein expression of HMGA 1 ,α-SMA but up-regulated expression of E-cadherin compared with TGF-β1 group and TGF-β1 + NC-siRNA group(P< 0 .05) .Conclusion HMGA1 interference could signifi-cantly down-regulate the expression of HMGA1 in LX-2 cells cultured with TGF-β1 ,thus inhibiting the proliferation and activation of the cells .

At present, the etiology and pathogenesis of multiple sclerosis are unclear. RIG-Ⅰ-like receptors are a new-ly discovered pattern recognition receptors (RLRs), which are located in cytoplasm. They can recognize the helicase of viral dsRNAs, and interact with interferon beta promoter stimulator (IPS)-1 through their caspase activation recruitment domain (CARD), then form IPS-1 signalsome and induce the expression of interferon typeⅠ(Ⅰ-IFN), thereby initiate innate im-mune response and induce antiviral response. Recent studies have found that mice lacking IPS-1 would develop exacerbated disease and accompanied by markedly higher inflammation, increasing axonal damage and demyelination. Furthermore, initi-ating the RIG-Ⅰ-like helicase receptor on the immune cells can alleviate inflammation and myelin fracture in multiple scle-rosis of mouse model, thus limit the incidence of paralysis. This paper is a review about the research progress on RLRs in the treatment of multiple sclerosis.