Abstract: Objective: To explore the effects of miR-125b on the proliferation and migration of cardiac fibroblasts via Toll-like receptor-4/nuclear factor-κB (TLR4/NF-κB) signaling pathway, and to clarify the role and mechanism of miR-125b in myocardial fibrosis. Methods: The HEH2 cells in logarithmic growth phase were randomly divided into blank control group, negative control group and miR-125b inhibitors group.The HEH2 cells in miR-125b inhibitors group were transfected with miR-125b inhibitors,and the HEH2 cells in negative control group were transfected with negative control inhibitors,and the HEH2 cells in blank control group were not transfected.The levels of miR-125b in the cells in various groups were determined by reverse transcription-polymerase chain reaction (RT-PCR) method.The proliferation activities of HEH2 cells were determined by MTTmethod.The Transwell chamber was used to measure the migration abilities of HEH2 cells;the expression levels of type Ⅰ collagen (Col Ⅰ), type Ⅲ collagen (Col Ⅲ), α-smooth muscle actin (α-SMA), TLR4 and NF-κB proteins in the HEH2 cells were determined by Western blotting method. Results: Compared with blank control group and negative control group, the level of miR-125b in the HEH2 cells in miR-125b inhibitors group was decreased (P<0.05), the proliferation activity and the number of migration cells were decreased (P<0.05), and the expression levels of Col Ⅰ, Col Ⅲ, α-SMA, TLR4, and NF-κB proteins were decreased (P<0.05).There were no significant differences in the miR-125b levels,the proliferation activities,the number of migration cells,the expression levels of Coll Ⅰ, Coll Ⅲ, α-SMA, TLR4, and NF-κB proteins in the HEH2 cells between blank control group and negative control group(P>0.05). Conclusion: Down-regulation of miR-125b level can inhibit the proliferation and migration of the cardiac fibroblasts, and its mechanism may be related to the TLR4/NF-κB signaling pathway.

Key words: miR-125b, Toll-like receptor 4, nuclear factor-κB, fibroblasts, myocardial fibrosis